The function of immune cells depends on specific mitochondrial metabolic programs that include nutrient oxidation, macromolecule synthesis and posttranslational modifications.[28] Studies have shown that HDAC3 promotes immune escape in breast cancer cells by downregulating microRNA-130a-3p and selectively inhibits lymphoma immune surveillance by activating HDAC3.[29,30] However, most mechanisms involved in gene regulation for immune modulation remain unclear and require further experimental exploration. The gene discussed is HDAC3; the disease is lymphoma.