Such significance of lipid homeostasis in AML LSCs is once again recapitulated as pharmacological inhibition of nicotinamide phosphoribosyltransferase (NAMPT), which depletes cellular nicotinamide adenine dinucleotide (NAD) and subsequently suppresses the conversion of saturated fatty acids to monounsaturated fatty acids, leads to the selective killing of LSCs over normal HSCs [167]. This evidence concerns the gene NAMPT and acute myeloid leukemia.