Furthermore, the interaction between AXL and 14-3-3ζ in hepatocellular carcinoma (HCC) leads to the phosphorylation of SMAD3 at Ser213, upregulating TGF-β target genes such as Snail, PAI1, and MMP9, and promoting autocrine TGF-β secretion.181 Studies on HCC further show that AXL overexpression drives metastatic progression by activating mesenchymal markers like Slug and Vimentin, contributing to sorafenib resistance.182 In colorectal cancer, increased AXL expression induces EMT and enhances resistance to polo-like kinase (PLK1) inhibitors via TWIST1 overexpression.183. The gene discussed is VIM; the disease is hepatocellular carcinoma.