Several potential mechanisms implicated in this EMT-induced CTX resistance are observed, such as (i) expression of lymphotoxin-b; (ii) methylation of EGFR that promotes the EGFR ligand-binding ability and dimerization (EGFR persistent activity) (169); (iii) secretion of CTX-containing extracellular vesicles, which lead to cancer cell protection (179); (iv) upregulation of EMT-related genes (133), especially by epigenetic regulation (170, 180); and (v) loss of the tumor suppressor gene SMAD4, which induces JNK and MAPK pathway activation (172, 173). This evidence concerns the gene EGFR and cancer.