Additional evidence supporting a pathogenic role of IgM in FSGS pathophysiology comes from recent studies demonstrating that combined B-cell and plasma-cell depletion with anti-CD20 and anti-CD38 antibodies effectively induced disease remission in multidrug-resistant FSGS and recurrent post-transplant FSGS.9 Notably, patients with IgM levels below the median at 3 months post-treatment exhibited a significantly lower relapse rate at 9 months than those with higher IgM levels, suggesting a mechanistic link between IgM and disease activity. The gene discussed is CD38; the disease is focal segmental glomerulosclerosis.