For example, miR-18a and miR-412 can negatively regulate ATM expression and reduce the number of tumor cells to repair DNA damage after radiotherapy [53,55]; miR-25 and miR-30d have been shown to interact with p53, the master regulator of DDR, and its down-regulation leads to the reduction of apoptosis via suppressing expression of its target genes (p21, BAX, Puma) [52]. This evidence concerns the gene BAX and neoplasm.