We demonstrated in an anti-glomerular basement membrane model of glomerulonephritis that iNKT cells modulate their pathogenesis through an alternative TGF-β signaling pathway, indicating a renoprotective role for TGF-β-iNKT axis and TGF-β-induced genes (TGFBI/BIGH3) [26]. Here, TGFBI is linked to glomerulonephritis.