CDKL1‐knockdown breast cancer cells were reported to be arrested at the G2/M phase and were more sensitive to cell cycle chemotherapeutic drugs.24 In addition, the CDKL1 level was considerably higher in GC tissues than in paired normal tissues, and CDKL1 silencing in GC cells decreased the amount of proliferating cell nuclear antigen and increased that of Bik pro‐apoptotic protein and then suppressed cell proliferation and induced apoptosis.25 Re‐analysis of a breast cancer GWAS study suggested that CDKL2 may contribute to cancer. The gene discussed is PCNA; the disease is breast carcinoma.