Knowing that BRG1 forms a functional regulatory unit with EP300 and that acetyltransferase is responsible for the BRG1-driven transcriptional activity of some cell-cycle-dependent genes, we aimed to determine whether the specific acetyl-lysine competitive protein–protein interaction inhibitor I-CBP112, which targets the bromodomain of the two closely related and highly homologous acetyltransferases CBP/EP300, could decrease the expression of multidrug-resistance proteins in the triple-negative MDA-MD-231 breast cancer cell line and thereby enhance the toxicity of anticancer drugs. This evidence concerns the gene EP300 and breast cancer.