Given that mice deficient in ALOX15 or treated with an ALOX15 inhibitor significantly suppressed the renal fibrosis by UUO [41], these results suggest that ALOX15 expression is enhanced by intracellular TG2 activity and induces M2 macrophage polarization, leading to pathological exacerbation of renal fibrosis. The gene discussed is TGM2; the disease is renal fibrosis.