The precise mechanism of resistance to sorafenib is unclear, as there are several mechanisms that contribute to this resistance, such as high EGFR and c-Jun expression, autophagy, hypoxia, epithelial-mesenchymal transition (EMT), tumor microenvironment, epigenetic regulation, ferroptosis, PI3K/Akt signaling pathway, Hippo/Yap pathway, and IL-6/STAT3 signaling, among others [47,48]. The gene discussed is AKT1; the disease is neoplasm.