Evolution of clonal hematopoiesis during treatment of persons with MCL. HSPCs acquire somatic mutations with aging, resulting in the production of a genetically heterogenous pool of HPSCs. Genotoxic stress induced by chemotherapy favors the selection of HSP-Cs carrying mutations of DNA damage response genes, such as TP53 and PPM1D (red cells). Auto-HCT induces replicative stress and potentially other stresses related to an altered bone marrow microenvironment. In this study, auto-HCT was associated with the selective expansion of HPSCs carrying DNTM3A R882 mutations (purple cells). During long-term follow-up, the existing clonal hematopoiesis was mostly stable.