The oncogenic action of FASN depends on the oncogene EGFR, which induces FASN hyperactivation in a bi-directional manner: i) maintaining incessant de novo fatty acid synthesis via FASN that awards lipogenic and micro-environmental metabolic adaptive benefits to pre-lesion oncogenesis, chemoresistance and metastasis in ovarian cancer [40]–[41]; ii) averting cellular toxicity arising due to end product of FASN action i.e. palmitic acid by conversion of excess fatty acids (FA) to triglycerides in PPAR-gamma dependent manner. This evidence concerns the gene FASN and ovarian carcinoma.