HCRT and acute myeloid leukemia: Studies using patient-derived xenograft (PDX) models revealed that araC-resistant AML cells overexpress genes driving OX/PHOS [39, 40], whereas murine syngeneic AML models have shown that residual cells increase the uptake of glutamine and aspartate to fuel OX/PHOS and synthesize pyrimidine and glutathione [41], which may represent adaptations required to survive in that context.