Aberrant alterations in microRNA expression lead to lymphomagenesis. Bromodomain and additional-terminal domain inhibitors for example OTX015 (MK-8628, birabresib) have shown preclinical and clinical activity in hematologic tumors. MicroRNA profiling of diffuse large B-cell lymphoma cells given OTX015 revealed alterations in the expression amounts of a restricted quantity of microRNAs, including miR-92a-1-5p, miR-21-3p, miR-155-5p and miR-96-5p. Analysis of openly available chromatin immunoprecipitation sequencing data of diffuse large B-cell lymphoma cells given bromodomain and additional-terminal domain (BET) inhibitors demonstrated the BET member of the family BRD4 certain to the upstream regulatory parts of multiple microRNA genes which this binding decreased following BET inhibition. Alignment in our microRNA profiling data using the BRD4 chromatin immunoprecipitation sequencing data says microRNAs downregulated by OTX015 also exhibited reduced BRD4 binding within their promoter regions following treatment with another bromodomain and additional-terminal domain inhibitor, JQ1, indicating that BRD4 contributes straight to microRNA expression in lymphoma. Treatment with bromodomain and additional-terminal domain inhibitors also decreased the expression from the arginine methyltransferase PRMT5, which plays a vital role in B-cell transformation and negatively modulates the transcription of miR-96-5p. The information presented here indicate that additionally to formerly observed effects around the expression of coding genes, bromodomain and additional-terminal domain inhibitors also modulate the expression of microRNAs involved with lymphomagenesis.