In this study, we tried to address this limitation by analysing the available chromatin accessibility data (ATAC-seq) generated in patient tumours from TCGA cohort, and identified differential accessible regions (that is, gained or lost chromatin accessible regions) in mutant p53 tumours compared to the wild-type p53 tumours, especially in breast infiltrating ductal carcinoma and colon adenocarcinoma. Here, TP53 is linked to neoplasm.