Indeed, the mTOR inhibitor rapamycin or BET bromodomain inhibitors were able to counteract some of the leukemogenic effects of mutated ASXL1. Finally, as the landscape of epigenetic aberrations and resulting dysregulated genes due to mutated ASXL1 and ASXL2 continue to be characterized, it is expected that therapeutic targeting of epigenetic regulators to restore the epigenome and transcriptome of HSC/HPCs will increasingly emerge as options to prevent progression of CHIP to the pre-leukemic myeloid malignancies or acute leukemia. This evidence concerns the gene MTOR and myeloid neoplasm.