RELB and cancer: Recently, Vallabhapurapu et al demonstrated that HDAC4 forms a complex with RelB and p52 proteins to promote cell growth by maintaining repressive chromatin at the promoters of proapoptotic genes Bim and BMF in cancer cells, while depletion of HDAC4 or treatment with the HDAC inhibitor TSA results in elevated mRNA levels of both BMF and Bim [30], which demonstrate that HDAC4 may directly influence transcription of specific genes by regulating deacetylation of histones.