By applying a PI-3 kinase inhibitor, YAP1 overexpression failed to induce upregulation of MRE11 and resulted in deactivation of CHK2, which ultimately failed to trigger DNA-damage repair in sh-ANKHD1 or sh-MALAT1 cells, suggesting that AKT was a crucial effector in regulating the ANKHD1/MALAT1/YAP1-loop-mediated radioresistance of CRC cells. This evidence concerns the gene MALAT1 and colorectal carcinoma.