Taken together, we observed that [1] CHK2 and its upstream kinases, ATR and DNA-PKcs are constitutively activated in OR CRC cells, [2] the higher basal levels of protein PARylation indicate that higher PARP1 activity is in OR CRC cells, and [3] other CHK2 downstream effectors, phospho-p53, phospho-CDC25C and γ-H2AX, are upregulated in some OR CRC cells. This evidence concerns the gene PARP1 and colorectal carcinoma.