While they are in a quiescent state or subjected to adverse tumor microenvironmental conditions such as limited glucose availability, CSCs may adapt by inducing a metabolic switch via the activation of the transcription factor, peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), to rely more heavily on OxPhos for ATP production [33,34]. Here, PPARGC1A is linked to neoplasm.