SETD2 and cancer: Loss of SETD2 also affected gene networks related to glucose, mitochondrial and fatty acid metabolism, including upregulation of PGC1α, a master regulator for cellular energy homeostasis [136], which could have induced oxidative phosphorylation and TCA cycle gene expression, an increase in mitochondrial mass, cell size, and intercellular complexity SETD2-deficient cells [135] demonstrating the role of this histone-modifying enzyme in metabolic reprogramming in cancer.