We show that both the compound mutant mice (Tet2–/–Ob/Ob and Dnmt3a+/–Ob/Ob) and the Ob/Ob mice that were transplanted with CHIP-mutant BM (Tet2+/–, Tet2–/–, Dnmt3a+/–, Asxl1+/–, and Jak2+/–) had exacerbated CH and a MPN-like phenotype. Here, ASXL1 is linked to myeloproliferative disorder.