This editorial provides insights into the pivotal role of checkpoint kinase 1 (CHEK1) as both a biomarker and therapeutic target in colorectal cancer (CRC), based on findings from a recent study by Pang . Using single-cell RNA sequencing and immunohistochemistry, the study demonstrates significant CHEK1 overexpression in CRC tissues and identifies nitidine chloride as a potent CHEK1 inhibitor that disrupts DNA damage repair pathways. These findings underscore the therapeutic potential of CHEK1 inhibition and highlight the need for further research to address gaps in CRC treatment.