SCD1 promotes liver cancer stemness through the synthesis of MUFAs, which can stabilise β-catenin, thereby inducing Wnt/β-catenin signalling, as well as generating a feed-forward loop to elevate SCD1 expression.115 SCD1 can also contribute to sorafenib resistance by inhibiting the endoplasmic reticulum stress-induced unfolded protein response.116 Importantly, suppression of SCD1 by a specific inhibitor not only sensitises the cells to sorafenib treatment but is also sufficient to suppress liver fibrosis and liver tumorigenesis. This evidence concerns the gene SCD and Hepatic fibrosis.