Metabolic strugGLS after FLT3 inhibition in AML

Abstract

In this issue of Blood, Gallipoli et al report that by performing an elegant clustered regularly interspaced short palindromic repeats (CRISPR) screen of FLT3 internal tandem duplication–positive (FLT3-ITD1) acute myeloid leukemia (AML) cells, they have identified that FLT3 inhibition exposes a therapeutically relevant metabolic dependency on glutaminolysis.