Through integrated RNA-seq and ATAC-seq analysis, we found that HDAC2 overexpression increases chromatin accessibility in BCa cells, promoting the transcription of the downstream GRIK2, which was previously reported as a target for bladder cancer stem-like cells (CSCs)/cancer-initiating cells (CICs)-targeting immunotherapy [27]. The gene discussed is HDAC2; the disease is urinary bladder carcinoma.