Loberg et al. established a DNMT3A-driven CHIP model in mice by transplanting Dnmt3aR878H/+ BM cells at a 50:50 ratio with wild-type (WT) CD45.1 BM cells and observed significant expansion of Dnmt3aR878H/+ HSPCs relative to Dnmt3a+/+ controls.18 Another BM transplantation (BMT) study, in which DNMT3A-driven CHIP was modeled with Dnmt3a−/− BM cells and linked CHIP to osteoporosis, involved the use of non-competitive BMT (100%Dnmt3a−/− BM cells).36 Since R50% is not a typical VAF in human CHIP,4,37 we transplanted a clinically relevant fraction (10%) of mutant BM cells. The gene discussed is DNMT3A; the disease is osteoporosis.