Given that most of the TET2 mutations in individuals with CHIP or in patients with chronic myelomonocytic leukemia (CMML), AML, or MPN are heterozygous in nature (TET2+/–), we next tested whether transplantation of a lower percentage of Tet2+/– pre-LHSCs/PCs (1:10 ratio) also results in their expansion at a higher rate in Ob/Ob FBM mice, similar to what we observed in Tet2–/– pre-LHSCs/PCs. Here, TET2 is linked to myeloproliferative disorder.