Importantly, the conclusion is supported by a metabolic-based response of AML-stroma co-cultures, up-regulation of acetate-processing enzyme ACSS2 (S30), acetate-enhanced leukemic growth with ACSS2 dependence, abolished leukemic metabolic fitness with ACSS2 mutant stroma and analyses of ACSS1/ACSS2-high mRNA expression in AML datasets. The gene discussed is ACSS1; the disease is acute myeloid leukemia.