In addition to fatty acids, MYC effectively reprograms cholesterol metabolism by upregulation of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR), the rate-limiting enzyme of cholesterol synthesis during malignant transformation.60 Moreover, it appeared that HMGCR is necessary for MYC phosphorylation and activation in some MYC-driven tumor models,61 arguing that a feedforward activation circuit between MYC and HMGCR promotes metabolic reprogramming and tumorigenesis. The gene discussed is MYC; the disease is neoplasm.