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The increasing complexity of the management of core-binding factor acute myeloid leukemia

of APY0201 was highest in patient-derived samples with hyperdiploidy (trisomies with one or more odd-numbered chromosomes) and lowest in patients’ samples with a t(11;14) translocation. In addition, ex-vivo samples with high TFEB levels were sensitive to APY0201. High TFEB levels have been associated with increased autophagic flux suggesting that autophagic flux may be directly related to PIKfyve inhibition. These preliminary results may suggest patient populations that could be enriched for in a future clinical trial. In conclusion, Bonolo de Campos et al. provide exciting data to support the ongoing investigation of therapeutically manipulating targets specific to plasma cell function, particularly protein handling in myeloma. Although the finer details of the actual mechanisms may differ somewhat between multiple myeloma and non-Hodgkin lymphoma, data from this study and those performed in nonHodgkin lymphoma provide compelling evidence for the role of PIKfyve inhibition in inducing cell death, with changes seen in the autophagy and lysosomal pathways. Notably, this study demonstrates the importance of the inherent genetic differences in myeloma biology and the potential role of PIKfyve inhibitors in targeting a distinct group of genetically defined myeloma to continue this era of personalized medicine. References