Yan and his colleagues found that specific knockout of endothelial MLKL in the NASH mouse model of hepatic fibrosis inhibited the activation of TGF-β/Smad 2/3 signaling pathway and reduced the degree of fibrosis, suggesting that endothelial MLKL could be a promising molecular target for the treatment of NASH fibrosis [76]. The gene discussed is MLKL; the disease is Hepatic fibrosis.