However, our subsequent studies found JTE-013 shows off-target inhibition of SPHK1 which contributes to its anti-AML effects [68], and that the loss of AML CSC survival induced by SPHK1 inhibition was actually caused by increased cellular ceramide levels causing an integrated stress response that induces loss of MCL1 [69]. This evidence concerns the gene MCL1 and acute myeloid leukemia.