The conserved CLEC10A pathway, the dose-responsive biomarker signature, and the favourable tolerability profile collectively argue that precision glyco-modulation may offer an orthogonal, immunometabolic route toward disease modification in human osteoarthritis and other degenerative disorders characterised by myeloid dysregulation—for example, erosive hand OA, diabetic tendinopathy, or even early post-traumatic joint degeneration. This evidence concerns the gene CLEC10A and osteoarthritis.