Although the above studies demonstrated a role of obesity in driving the growth of Tet2- and Dnmt3a-mutant HSC/Ps and a MPN-like phenotype in transgenic mice, we next sought to explore whether obesity contributes to CH and whether the expansion of mutant HSC/Ps is driven by FBM in a microenvironment-dependent manner. Here, TET2 is linked to myeloproliferative disorder.