SLC5A3 and acute myeloid leukemia: Recurrent transcriptional silencing of ISYNA1 might largely contribute to the SLC5A3-mediated myo-inositol dependency in AML patients, since gain- and loss-of-function experiments were employed to unveil a synthetic lethal genetic interaction between ISYNA1 and SLC5A3 (148), indicating that combined treatments with SLC5A3 and ISYNA1 inhibition together could be exploited in AML.