Telomerase, reverse transcriptase, tumor protein 53, and β-catenin are the genes that are most frequently involved in mutations that lead to oxidative stress in HCC [26]. Molecular pathways responsible for HCC include the dysregulation of many signal transduction pathways, such as p53, Ras, Wnt/β-catenin, MAPK (mitogen-activated protein kinase), an activator of transcription (STAT), Janus kinase (JAK)/signal transducer, phosphatidylinositol 3- kinase (PI3K)/Akt, hedgehog, TGF-beta, and epidermal growth factor [27,28]. The gene discussed is SOAT1; the disease is hepatocellular carcinoma.