Noticeably, wild‐type p53 establishes the G1/S checkpoint primarily through transcriptionally activating p21,[5, 38] whereas p27 becomes essential for maintaining the control only when the initial wave of p53‐driven p21 activity is diminished.[11] As such, a biological model has been proposed where p27 controls the G1/S checkpoint in cancer cells lacking an active p53/p21 pathway.[11, 39] Therefore, in wild‐type p53 CRC cells under steady‐state conditions, p53/p21 signaling overrides p27 signaling even when p27 is upregulated in cells with LIMp27 knocked down. This evidence concerns the gene CDKN1A and cancer.