In another study, it was reported that mouse models of CH carrying mutations in Tet2, Dnmt3a, Asxl1, and Jak2 demonstrated that obesity accelerated the size of CH clones and increased the risk of developing a myeloproliferative neoplasm (MPN)-like phenotype, regardless of the specific mutation[40]. This evidence concerns the gene DNMT3A and myeloproliferative disorder.