In normal B cells, EphA7 S acts as a tumor suppressor by dominant-negative inhibition of dimerization and activation of oncogenic EPHA2 and our data suggest that BMI1 overexpression may contribute to the development of tumors such as B-cell derived follicular lymphomas by repressing EPHA7 S. Despite the upregulation of EphA7 variants in Bmi1−/− cells and tissues, no attenuation of the altered spleen, thymus and bone marrow parameters and the abnormal cerebellar anatomy was observed in Bmi1−/−/EphA7−/− mice. Here, EPHA2 is linked to neoplasm.