Contrary to the conventional evidence, a study by Farge et al. revealed that CD34+CD38− cells from BM of AML patient-derived xenograft (PDX) models neither increased nor exhibited a predominantly quiescent phenotype following AraC administration, and that the elevated OXPHOS machineries observed in chemo-resistant leukemic cells are specifically mediated by fatty acid oxidation [164]. The gene discussed is CD38; the disease is acute myeloid leukemia.