Editorial Volume 11, Issue 12 pp 3895—3897

Figure 1. Phospholipid metabolism regulates AML growth and stemness. Loss of tafazzin (TAZ) reduces cardiolipin (CL) level and causes subsequent dysfunction of phosphatidylserine decarboxylase (PISD), which in turn increases intracellular levels of PS. PS suppresses acute myeloid leukemia (AML) stemness and induces AML differentiation through activation of Toll-Like Receptor (TLR) pathway. PISD inhibitor, genetic knockout of PISD or supplementation of PS result in the same therapeutic effect, suggesting increasing PS is a potential therapeutic strategy for AML.