Recent studies have further shown that IRF4 is critical for the class-switch recombination by inducing activation induced deaminase and for germinal center reaction by downregulating Bcl6. IRF4 has been found to induce c-Myc expression in multiple MDV3100 myeloma cells and is critical for their survival and expansion. Finally, IRF4 can induce the expression of Fas apoptosis inhibitory molecule to regulate mature B cell survival and apoptosis. Given its role as a critical transcriptional regulator that limits pre-B cell expansion and promotes pre-B cell differentiation, it is reasonable to assume that IRF4 may function as a tumor suppressor against pre-B cell transformation. Indeed, a previous study has shown that IRF4 functions as a tumor suppressor to inhibit BCR/ABL oncogene induced B cell acute lymphoblastic leukemia. In addition, mice deficient for both IRF4 and IRF8 develop lymphoblastic leukemia. Although IRF4 can suppress BCR/ABL induced B cell transformation, the molecular mechanism by which IRF4 exerts its function remains unclear. In this report, we assessed the role of IRF4 in c-Myc oncogene induced B cell transformation by breeding IRF4 deficient mice with EmMyc transgenic mice. In the EmMyc mice, the expression of c-Myc oncogene is driven by immunoglobulin heavy chain enhancers and is predominantly found in the B cells. EmMyc transgenic mice mainly develop two types of leukemia/ lymphoma: pro/pre-B derived and mature B cell derived and the majority of the EmMyc mice succumb to disease within 5 to 6 months of age. It has been shown that the leukemogenesis of EmMyc mice can be modulated by oncogenes and tumor suppressor genes and thus, EmMyc mice have been widely used as an animal model to assess the role of potential oncogenes or tumor suppressor genes in B cell transformation. In this report, we show that c-Myc induced leukemia was greatly accelerated in the IRF4 heterozygous mutant mice. Moreover, we provided evidence that IRF4 functions as a classical tumor suppressor gene to inhibit c-Myc induced leukemogenesis. The transforming growth factor-b signaling pathway plays an important role in controlling proliferation, differentiation, and other cellular processes including the growth of ovarian surface epithelial cell. Dysregulation of TGFb signaling is frequently observed in epithelial ovarian cancer and may be crucial to EOC development. The effects of TGFb are mediated by three TGFb ligands — TGFb1, TGFb2 and TGFb3, acting through TGFb type 1 and type 2 receptors. TGFBR2 is the specific receptor for TGFb ligands.