While preliminary evidence identifies ferroptosis as a key pathogenic factor in IgA nephropathy—linked to GPX4 downregulation, Gd-IgA1-induced mesangial cell injury, and the PPARα–FABP1–ACSL4 regulatory axis—and validates ferroptosis inhibitors as potential therapeutics, several critical, insufficiently addressed research gaps persist. The gene discussed is ACSL4; the disease is IgA glomerulonephritis.