BNIP3 and cancer: We also hereby define a novel molecular mechanism by which BNIP3‐driven autophagy sustains oral CSC progression and metastasis under hypoxic conditions through a mixed glycolytic/OXPHOS metabolism with a prevalent increase in OXPHOS levels, pushing them to become more reliant on mitochondrial oxidative metabolism for survival, and further targeting of this pathway could restrict the survival of CSCs, resulting in the development of new therapeutic strategies for cancer cells.