In addition, we found that UUO-induced Sphk1 expression was remarkably reduced in Tnfsf14 KO mice, and in vitro recombinant TNFSF14 administration markedly up-regulated Sphk1 expression of mTECs, indicating TNFSF14 was required for Sphk1 production during renal fibrosis and TNFSF14 may mediate renal fibrosis by way of potentiating pro-fibrotic factor Sphk1 expression. This evidence concerns the gene TNFSF14 and renal fibrosis.