In previous studies, genetic modifications of mice with conditional ablation of S100a8 gene in myeloid cells or general knockout of S100a9 gene have exhibited beneficial effects in glomerulonephritis and obstructive nephropathy due to the inhibition of inflammatory response.[33, 34, 35] Yet in a bIRI (bIRI) mouse model, sustained S100a8/a9 deficiency by S100a9 knockout shows detrimental effects leading to renal fibrosis and damage.[36] However, we observed a recovery of survival rate and improved renal function after small molecule inhibition of S100a8/a9 signaling in bIRI mouse model. The gene discussed is IGKV1D-22; the disease is glomerulonephritis.