Just a quick addition that I forgot to mention, I would consider...

Just a quick addition that I forgot to mention, I would consider when sleeping to keep one eye open on Multiple Sclerosis.
Although DMD research and testing is doing all the current heavy lifting and will bring financial benefits, MS has been a heavy lifter in the past and is just humbly sitting behind DMD benefitting from results and trials and research and knowledge.
The MS trial from ANP in my opinion had spectacular results but was stymied in some part by funding and regulatory safety processes.
A lot of data coming out of the DMD research may also have some correlation to the advancement in understanding the functionality and workings of ATL-1102 in Multiple Sclerosis, particularly in relation to Lesion growth/reduction.
CXCL16 is a very relevant aspect in relation to MS and lesions.
Some snippets that may suggest correlations:
(and I add that these snippets are just to show that there is a significant relationship between MS lesions and CXCL16)
Conclusions

mce-anchor
Serum levels of CXCL16, MMP-9, and osteoprotegerin reflect disease activity in MS, but are not affected by ω-3 fatty acid treatment. CXCL16 could be a novel biomarker and potential predictor of disease activity in MS.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0075021

The chemokine CXCL16 and its receptor, CXCR6, are also very important mediators of EAE development and Th17 cell interactions with neutrophils. CXCL16 is expressed by antigen-presenting cells such as monocytes, macrophages, B cells, and dendritic cells [34]. We found high levels of this chemokine in mouse brains, and moreover neutrophils demonstrated an increased expression of CXCR6. The elevated CXCL16 production in the EAE brain may help to recruit CXCR6+ cells across the BBB into gray matter foci, but additional, unknown signals provided during injury are required for gray matter infiltration [35]. It has been shown that administration of neutralizing antibodies against CXCR6 reduced EAE severity and inflammatory cell infiltration of the CNS [36].
https://www.hindawi.com/journals/mi/2014/590409/

The Effect of Scavenger Receptor Knockdown on Myelin Phagocytosis In Vitro

As this study and our earlier work (14) revealed high expression of scavenger receptors in the rim as well as around chronic active MS lesions, we studied the role of OLR1, CD68, MSR1, and CXCL16 in an in vitro myelin phagocytosis assay (Figure 6). Antisense oligonucleotides were developed that downregulate expression of these genes in the human macrophage cell line THP-1, confirmed by qPCR (Figure 6A). Immunocytochemistry confirmed the efficient knockdown of MSR1 (Figure 6B). Knockdown of MSR1 and CXCL16 significantly decreased the percentage of macrophages that phagocytosed myelin and the total myelin phagocytosed, compared to untreated cells (Figure 6C). Phagocytosis of myelin derived from control or MS tissue was similarly reduced by MSR1 knockdown (Figure 6D). To block scavenger receptor function in a redundant manner, we also applied a broad pharmacological inhibitor (22, 23). Fucoidan showed a non-toxic, dose-dependent significant reduction of the percentage of macrophages that phagocytosed myelin and the total amount of myelin phagocytosed at 1,000 µg/ml (p = 0.007; Figure 6E). Upregulation of scavenger receptors in chronic active MS lesions thus likely contributes to demyelination.

Scavenger Receptors Upregulated in and around Chronic Active MS Lesions Mediate Myelin Uptake

Myelin uptake during demyelination likely depends on scavenger receptors. We found OLR1, CD68, MSR1, and CXCL16 upregulated in all three comparisons (CXCL16 only in comparison I and in comparison II with qPCR). Thus, these scavenger receptors are upregulated in chronic active rims, but also around chronic active lesions, indicating that they are involved in early demyelination. We cannot fully exclude some contamination of PL regions with rim tissue during laser dissection, but early demyelination around chronic active lesions is further indicated by immunohistochemistry, showing upregulation of CHIT1, GPNMB, and OLR1 in and around chronic active MS lesions. These results extends our earlier work, showing enhanced expression of CD68, MSR1, and CXCL16 in and around chronic active MS lesions, compared to control tissue (14). CD68 is a scavenger receptor predominantly expressed on the lysosomal membrane, but the small percentage expressed on the plasma membrane is capable of oxLDL phagocytosis (38, 39). SA-RI/II, encoded by MSR1, was shown to be directly involved in myelin uptake in vitro (40–42), and Msr1^−/− mice showed less severe disease and reduced demyelination in the EAE model (43). CXCL16 has a dual function as a scavenger receptor and as a chemokine in soluble form. Neutralizing antibodies against CXCL16 delayed the onset and reduced the severity of EAE in mice (44). The soluble form is elevated in MS patients, compared to control subjects (45). This indicates that scavenger receptors could be actively involved in demyelination in MS. Furthermore, their upregulation in the PL-NAWM of chronic active MS lesions, might suggest they are involved in the initial stages of MS lesion development and progression.
The functional role of OLR1, CD68, MSR1, and CXCL16 was studied in an in vitro myelin phagocytosis assay, using the human macrophage cell line THP-1. All genes were significantly downregulated, compared to untreated cells. Downregulation of MSR1 and CXCL16 resulted in a significant decrease in the number of myelin-phagocytosing cells and total myelin uptake. A direct role of MSR1 in myelin phagocytosis in MS is consistent with earlier research (40–42) and supported by its expression in regions of active demyelination in MS brain tissue. Its upregulation in the PL-NAWM of chronic active MS lesions could indicate that phagocytosing cells in yet unaffected areas are already preparing for demyelination. Notably, pharmacological inhibition of a broad spectrum of scavenger receptors by fucoidan further reduced the number of phagocytosing macrophages and the total amount of myelin uptake, indicating that a combination of scavenger receptors contributes to the uptake of myelin.

https://www.frontiersin.org/articles/10.3389/fimmu.2017.01810/full?report=reader