In general, aberrant ID expression seems to favor proliferation, to inhibit differentiation, and to facilitate tumor neoangiogenesis.[2] From early B-cell development to mature B cells, E2A is the first one of the three transcription factors (E2A, EBF, and PAX5) to be expressed, and E2A together with EBF regulates the expression of PAX5.[3,4] The inhibitor of DNA binding ID2 (inhibitor of DNA binding 2 or inhibitor of differentiation, ID2), may bind and negatively regulate E2A and PAX5[5,6] by direct interaction. This evidence concerns the gene ID2 and neoplasm.