A major hallmark of cancer cells is their ability to reprogram metabolism to sustain the energetic and biosynthetic demands of continuous proliferation.18 In PDAC, mutated KRAS has been identified as a key driver of metabolic reprogramming.19,20 Notably, mutant KRASG12D has been shown to increase glycolysis, which, for example, fuels ribose biogenesis through increased flux into the nonoxidative pentose phosphate pathway.19 The gene discussed is KRAS; the disease is cancer.