Ann: US FDA Type C Meeting for ATL1102 in DMD, page-31

My take is that it is a professional restrained response from ANP saying "all went well"
I think the previous tox aspect concerns were greatly diminished with the MS and DMD trials and no adverse effects, at greatly varying doses. The fact there has been no inkling of JCV or PML at some point has to be taken on merit, supposition regarding a concern is not evidence.
Also, the below may suggest why ATL-1102 may not stimulate adverse effects.

More analysis is required to characterize the pharmacologic and pharmacodynamic action of ATL1102. This also extends to ascertaining the profile of ATL1102 with respect to the risk of PML. Natalizumab increases the release of CD34+ hematopoietic stem/progenitor cells and CD19+ pre B cells and CD20+ B cells into the blood, which carry latent low copy JC virus,^30,31 including in individuals who are seronegative.³¹ Latent JC virus activation is theorized to involve B-cell differentiation, including B-cell DNA-binding protein Spi-B, which increases JCV transcription.³⁰ Natalizumab has a long half-life in the blood (6 days), and a broad VLA-4 antagonist effect, and can impair JC virus immunosurveillance, leading to PML.^4,30
Preliminary data have shown ATL1102 treatment increases CD34+ RNA 50% at week 8 vs baseline, though its effects at the CD34+ cell level need to be explored¹⁴ (appendix e-2). The reduction of CD19+ (pre) B cells with ATL1102 treatment suggests that release of lymphoid precursors into the blood may be low or they do not survive, potentially reducing the pool of cells that may carry latent virus. ATL1102 does not bind cell surface VLA-4. Natalizumab binding to VLA-4 induces intracellular signaling–associated proinflammatory effects, leading to poor outcomes in patients with PML following treatment suspension.^30,32 The short ATL1102 half-life in plasma of 4.8 hours¹⁴ potentially limits exposure of circulating leukocytes to drug, which may better preserve blood leukocyte VLA-4–mediated immunosurveillance and therefore be at less risk of causing PML. IFN-β1 treatment of RRMS reduces blood mononuclear cell CD49d RNA³³ and VLA-4 expression on CD8+ lymphocytes³⁴ and CD4+CD45RO+ primed memory T cells, while preserving other blood leukocyte VLA-4 function.³⁵ IFN-β1 has not been associated with PML.

Also, non-clinical can be varying, and the highlighted below could suggest logistics, etc rather than product reaction.

The meeting was constructive and provided clarification on a path towards initiating a Phase IIb/III study in the US. Non-clinical requirements are to be further reviewed and agreed with the FDA to assess if and how they may impact on the timing of clinical study initiation.

Obviously Mark cant be as specific as he'd like, nothing can be stated precisely until notes are received, but i read that the path forward has been designed, all we have to do is meet that design, and with the team with have i believe that it will be achieved.
All in all a great progress report.