MEF2B是致癌基因，编码蛋白是一种转录激活因子，参与肌肉特异性基因表达，其在介导心脏和骨骼肌的分化中起作用。MEF2B调节促进细胞迁移和上皮-间充质转变的转录程序，类似癌基因MYC、TGFB1、CAD11、RHOB和NDRG1。MEF2B在人细胞系中的过度表达导致细胞迁移增加。 MEF2B在卵巢浆液性囊腺癌、肾上腺皮质癌和食管癌等多种癌症类型中发现扩增。在弥漫性大B细胞淋巴瘤（DLBCL）、滤泡性淋巴瘤（FL）和套细胞淋巴瘤（MCL）中发现了MEF2B的复发性体细胞突变。DLBCL中MEF2B的突变导致BCL6的转录增加，BCL6是DLBCL生发中心增殖所必需的原癌基因，并且与共抑制因子CABIN1的关联性降低。然而，其他数据表明MEF2B突变导致DNA结合的丧失和DLBCL细胞趋化性的降低。

MEF2B, a transcriptional activator, is altered by mutation in various hematological malignancies including follicular lymphoma.MEF2B is a transcription factor that has a role in mediating differentiation in heart and skeletal muscle. MEF2B regulates transcriptional programs that facilitate cell migration and epithelial-mesenchymal transition as well as the cancer genes MYC, TGFB1, CARD11, RHOB and NDRG1. Consistent with a role in epithelial-mesenchymal transition, overexpression of MEF2B in human cell lines results in increased cell migration. MEF2B has been found to be amplified in several cancer types including ovarian serous cystadenocarcinomas, adrenocortical carcinomas and esophageal carcinomas. Recurrent somatic mutations in MEF2B have been identified in diffuse large B-cell lymphoma (DLBCL) , follicular lymphoma (FL) and mantle cell lymphoma (MCL). The recurrence of MEF2B mutations at particular residues is consistent with the notion that MEF2B mutations have either gain-of-function or dominant negative effects on MEF2B activity. Mutations in MEF2B in DLBCL lead to increased transcription of BCL6, a proto-oncogene essential for DLBCL germinal center proliferation and decreased association with the co-repressor CABIN1. However, other data suggest that MEF2B mutations lead to loss of DNA binding and decreased DLBCL cell chemotaxis.

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