Several tumor-intrinsic factors have been associated with resistance to cTACE, including activation of the NRF2 antioxidant pathway,11 overexpression of pyruvate kinase M2 (PKM2),12 and activation of the HIF1α/pAKT signaling loop.13 These pathways promote tumor cell survival under stress conditions, such as hypoxia and nutrient deprivation induced by TACE. The gene discussed is HIF1A; the disease is neoplasm.