While such metabolic profile is appreciated in sterile inflammatory responses to implanted biomaterials21–23,45,61, it is still uncharacterized in cancer biology, and has only been documented in a resistant clone of PDAC cancer stem cells (CSC) where suppression of MYC and increase in PGC-1α underlie increment in both OXPHOS and glycolysis62. The gene discussed is PPARGC1A; the disease is cancer.