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CD19- and B-cell maturation antigen (BCMA)-directed chimeric antigen receptor T-cell (CAR T-cell) therapies have improved outcomes in relapsed or refractory B-cell lymphoid malignancies and multiple myeloma, but late hematologic complications are increasingly relevant as survivorship expands. This narrative review examines how pre-infusion clonal hematopoiesis (CH), clonal hematopoiesis of indeterminate potential (CHIP), clonal cytopenia of undetermined significance (CCUS), marrow reserve, prior genotoxic exposure, inflammatory stress, and disease-platform context shape the risks of prolonged cytopenia and therapy-related myeloid neoplasms (t-MN) after CAR T-cell therapy. Available evidence suggests that high-risk clonal architecture, particularly TP53-mutated or DNA damage response-associated clones, clonal cytopenia, larger or multiple clones, and heavy prior cytotoxic exposure, is more clinically informative than CHIP positivity alone. By contrast, associations between unstratified CH and prolonged cytopenia remain heterogeneous. CD19 lymphoma and BCMA myeloma settings share clonal-selection biology but differ in marrow ecology, treatment history, baseline cytopenia, inflammatory burden, and surveillance windows. For clinical translation, risk assessment should not rely on universal CHIP screening or binary genomic classification. Instead, clonal-risk models, hematotoxicity-risk models, baseline blood counts, inflammatory markers, prior therapy exposure, and disease-platform context should be integrated to identify patients who may benefit from intensified myeloid surveillance, supportive-care planning, and earlier marrow reassessment while preserving access to CAR T-cell therapy.