PPARGC1A and acute myeloid leukemia: In this context, NOX2 and PGC-1α could be interesting targets, as (1) NOX2 knocked-down AML blasts have reduced mitochondrial respiration; (2) the NOX2 inhibitor decreases mitochondrial transfer and AML cell viability, whereas it is ineffective on normal HSCs, and (3) inhibition of PGC-1α in BM-MSCs reduces mitochondria transport (159).