Interestingly, the expression of the rate-limiting enzyme in the synthesis of β-hydroxybutyrate, 3-hydroxy-3-methyl glutaryl CoA synthase 2 (HMGCS2), is repressed by the oncogene c-Myc [8], and SIRT3, associated with tumor suppression function, is responsible for the maintenance of HMGCS2 in the deacetylated state, thus keeping the enzyme in optimally active form [9]. The gene discussed is HMGCS2; the disease is neoplasm.