Consistent with these findings, our custom analysis of published data showed that a pharmacological inhibition of ACLY in prostate cancer cells (63) phenocopied both SLBP downregulation and histone mRNA polyadenylation, a potential indicator for the decrease of histone transcripts as observed in 53BP1-deficient cells in this study (Supplementary Fig. S14 and Supplementary Table S4). The gene discussed is TP53BP1; the disease is prostate carcinoma.