In cells with high rates of aerobic glycolysis, such as some cancers, βOHB that is not/cannot be metabolized oxidatively instead accumulates in the nucleus where its HDAC inhibiting activity down-regulates GLUT1 expression and promotes cell death and apoptosis pathways (Li et al., 2006; Donohoe et al., 2012; Rodrigues et al., 2017). This evidence concerns the gene HDAC9 and cancer.