Fighting fat in AML

Abstract

In this issue of Blood, Dany et al demonstrate a critical role of the ceramide-regulated signaling pathway in inducing mitophagy to cause cell death and overcome drug resistance of acute myeloid leukemia (AML) cells carrying internal tandem duplication (ITD) of the Fms-like tyrosine kinase 3 (FLT3) gene.1 Inhibition of FLT3-ITD signaling through altering ceramide-involved lipid metabolism provides a new strategy for treating FLT3-ITD-positive AML and overcoming drug resistance by pharmacologically blocking FLT-3-ITD downstream signaling to enhance ceramide-mediated mitophagy.