In this study, bioinformatics analysis using the ENCODE database, followed by ChIP assay showed that H3K27ac was highly enriched at the promoter of MyD88, and this histone acetylation was mediated by AGAP2-AS1 as evidenced by the fact that the enrichment level was influenced by AGAP2-AS1 expression in the breast cancer cells. Here, MYD88 is linked to breast carcinoma.