These findings signify that 1) the circulating levels of sFasL remain the same despite cisplatin-induced renal damage, 2) urinary excretion of sFasL is associated with cisplatin-induced AKI, 3) kidney is the primary source of urinary sFasL in cisplatin-treated mice, and 4) renal oxidative stress promotes renal mFasL shedding. This evidence concerns the gene FASLG and acute kidney injury.