Notably, restoring miR-200c expression either in normal mammary epithelial cells overexpressing p53 mutants or in BLBC cells harboring endogenous MTp53 not only counteracts MTp53-induced EMT and stemness, but also recovers the decreased OXPHOS activity, foretelling the promising future of treating cancers with p53 mutation by modulating the mediators of metabolic reprogramming indirectly driven by MTp53. Here, TP53 is linked to cancer.