Moreover, the knock down of two enzymes that are responsible for the generation of cytosolic Ac-CoA (cytosolic enzymes ATP citrate lyase (ACLY)) and the cytosolic form of the acetyl-CoA synthetase ACSS2 [41,46,47]) enables the reduction of the acetylation of HIF1α and caused an accumulation of normoxic HIF1α independent of glutamine/ammonia-induced treatment in different tumor cell lines (Figure 4). The gene discussed is ACLY; the disease is neoplasm.