Another paper recently showed that ASXL1 mutations, which are often associated with lower PTEN levels, exhibit significantly higher sensitivity to the AKT inhibitor MK2206, consistent with the fact that excessive PI3K/AKT/mTOR activation may be a direct consequence of HMAs targeting the general mechanism of transcriptional repression (hence protection of chromatin structure) as well as AML cell survival [31]. The gene discussed is MTOR; the disease is acute myeloid leukemia.