We have several supporting lines of evidence supporting our model: (1) detectable CH tends to co-occur in the same individuals with elevated mtDNA SNV burden (who also tend to have an elevated hematologic cancer risk), (2) common germline variants in genes such as TCL1A and TERT that are strongly implicated in CH are also associated with mtDNA SNV mutation accrual, and (3) gene-based analyses identify coding mutations in numerous known CH driver genes as co-occurring in those with high mtDNA SNV burden. Here, TERT is linked to hematopoietic and lymphoid cell neoplasm.