Taken together, the striking consistency among our in vitro and in vivo results, as well as clinical validation strongly supports our model that Mutp53 potentiates FAO through constitutively upregulating CPT1C via dysregulating the miR-200c-ZEB2 axis, which in turn facilitates EMT-associated phenotypes, enhances cancer stemness, and promotes metastasis through modulating cellular redox status, leading to the progression of BLBC and the poor clinical outcomes in BLBC patients (Figure 7I). The gene discussed is ZEB2; the disease is cancer.