While suitable targets for this disease may not yet be apparent as the underlying pathophysiology remains incompletely understood, the reported mechanisms leading to IgAV nephritis are strikingly similar to those described in IgA nephropathy with galactose-deficient IgA1 acting as a key antibody for immune complex formation, there therefore may be repurposing opportunities.98 The gene discussed is IGHA1; the disease is IgA glomerulonephritis.