TPM-normalized transcription of each gene was significantly upregulated by BRD9 inhibition (P = 0.0001, P = 0.0044, P = 0.0043 for Ppp1r13b, Polβ, and Btg1, respectively), indicating possible roles for the BRD9 bromodomain in suppression of DNA repair and cell-cycle checkpoint evasion in AML. The gene discussed is BTG1; the disease is acute myeloid leukemia.