Regarding ADR + vehicle-treated mice, although the increase in plasma creatinine levels was not significant, strong urinary albumin excretion, low expression of WT1, and a high degree of glomerulosclerosis were clearly prevented by SRT1720 chronic administration, suggesting that SIRT1 contributes to attenuating the progression of glomerular injury in the experimental model of ADR-induced FSGS. The gene discussed is SIRT1; the disease is focal segmental glomerulosclerosis.