The dysregulation of receptor tyrosine kinases (RTK) such as epithelial growth factor receptor (EGFR), c-Met, and HER2 often occurs in HCC, which subsequently contributes to constant activation and autophosphorylation of a wide range of downstream signaling pathways such as RAS/MAPK, PI3K/AKT, and JAK2/STAT signaling, thereby driving cell proliferation in HCC [16]. This evidence concerns the gene SOAT1 and hepatocellular carcinoma.