Additionally, the role of non-classical ferroptosis regulators (e.g., FSP1, DHODH, and GCH1/BH4) in IgA nephropathy is entirely unexplored; whether these radical-trapping antioxidant pathways compensate for GPX4 downregulation in affected kidneys or if their dysfunction exacerbates ferroptosis susceptibility remains unknown, limiting multi-targeted therapeutic design. The gene discussed is GPX4; the disease is IgA glomerulonephritis.