,11 Interestingly, forced expression of a truncated ASXL1 protein predicted from the frameshift mutation could also promote the development of myeloid malignancies in a transgenic mouse model, suggesting a potential pathological function of the putative truncated protein, although such proteins remain to be detected in patients.12, 13, 14, 15 Suppression of EZH2 activity has been proposed as a key oncogenic function associated with ASXL1 mutation,15,16 which is consistent with the findings of EZH2 LoF mutation in ∼10% of patients with MDS/MPN and CMML.17 Here, EZH2 is linked to myeloproliferative neoplasm.