In another study, BAX overexpression in the T-cell lineage enhanced lymphomagenesis in TP53-deficient mice in a dose-dependent manner, and even initiated lymphoma formation on a TP53-proficient background.59 In accordance with data discussed before, BAX-driven apoptosis led to increased chromosome instability, and co-expression of BCL-2 was able to delay lymphomagenesis. This evidence concerns the gene TP53 and lymphoma.