BCL2 and neoplasm: Such mice did not develop a B cell malignancy without alloantigen stimulation, but when crossed with two lymphoma models (c-MYC and BCL2), the E571K mutation enhanced the lymphomagenic potential of c-MYC and BCL2, suggesting additional molecular abnormalities must be present for the E571K XPO1 mutation to incite an aggressive tumor progression [24].