In conclusion, our present work unravels the previously unconfirmed function of Mutp53 in FAO, depicts the detailed molecular mechanism accounting for Mutp53-mediated metabotypes, and uncovers the novel biological roles of CPT1C in cancer progression, which is not only a milestone for the thorough understanding of the p53 regulatory network of metabolism but also an indication that targeting Mutp53-miR-200c-ZEB2-CPT1C axis might be developed into a novel and effective therapies for BLBC in the imminent future. The gene discussed is ZEB2; the disease is cancer.