In our previous study, PDCD11 was confirmed to be overexpressed in p53‐wild‐type (p53‐WT) colon cancer cells with an “extra‐nucleolar” distribution, which facilitated the recruitment of p53 to HDM2, thereby destroying p53 to accelerate G2/M transition and tumor growth.[11] Here, the expression and distribution patterns of PDCD11 did not change in p53‐mutant breast and colon cancer cells, but switched to initiate C‐MYC‐regulated transcription. The gene discussed is TP53; the disease is colonic neoplasm.