Our findings establish that breast cancer cells possess a dynamic degree of plasticity that enables them to readily switch between glycolytic and autophagic phenotypes (Fig. 6); they also show that simultaneous inactivation of both survival mechanisms may offer new inroads into eliminating dormant disseminated breast cancer cells, findings reminiscent of those employing dual targeting of Pfkfb3 and mitophagy/autophagy to alleviate mitotic-arrested breast cancer cells49. Here, PFKFB3 is linked to breast cancer.