Our observation that TSPAN32 downregulation is widespread across T-ALL, B-ALL, and CLL suggests a broadly conserved oncogenic program; however, the lack of TSPAN32 repression in a subset of patients implies that specific genetic lesions—or compensation by alternative transcriptional networks—may preserve TSPAN32 expression in certain contexts. The gene discussed is TSPAN32; the disease is B-cell chronic lymphocytic leukemia.