In line, assessment of lymphomas from B6-STIL control, CMV-STIL+/- and CMV-STIL+/+ mice by Ki67 immunostaining revealed that, corresponding to STIL protein levels, proliferation rates were elevated independent from lymphoma genotypes (Fig 5F), suggesting that translational shutdown of STIL transgene expression has occurred in lymphomas as well and STIL protein expression is a consequence of increased lymphoma cell proliferation. This evidence concerns the gene MKI67 and lymphoma.