One study using a cisplatin-induced acute kidney injury model showed that TNFR2-deficient mice had milder kidney injury compared to TNFR1-deficient mice after cisplatin treatment [63] Moreover, another study has found that among unilateral ureteral obstruction (UUO) mice, TNFR1 knockout mice had less severe renal lesions, such as collagen IV deposition, α-smooth muscle actin (α-SMA) matrix score, and NF-κB activity, than TNFR2 knockout mice [64]. This evidence concerns the gene TNFRSF1A and acute kidney injury.