Considering two lines of evidences showing that: (1) phosphatase and tensin homolog (PTEN), a lipid phosphatase that antagonizes the phosphatidylinositol 3-kinase pathway, was enriched in BCL6 promoter binding peaks in primary germinal center B cells (Ci et al., 2009), and that (2) BCL6 directly binds to the promoter locus of PTEN in patient-derived acute lymphoblastic leukemia (Geng et al., 2015), we hypothesized that an increase in BCL6 expression by genotoxic stress might inhibit PTEN and subsequently promote cell survival. The gene discussed is BCL6; the disease is acute lymphoblastic leukemia.