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Biomarkers are a surrogate for clinical response.
Inflammation causes surges in CRP, ferritin, WCC, etc.

But serologic biomarker levels can be altered in the absence of a clinical response. So they will never be superior to a clinical endpoint.

For example, creatinine is used as a marker of renal function. When someone's kidneys are struggling creatinine increases.

But if someone's on trimethoprim for an infection, it competes with the excretion of creatinine and raises the level in the absence of renal impairment.

So, theoretically, if someone takes an immune-modulating therapy that decreases CRP production (or increases its excretion) but doesn't actually dampen inflammation, CRP would not be a relevant endpoint. Clinical response would be the key in that case.