Considering that PDCD11 exhibits an “extra‐nucleolar” distribution in p53‐WT colon cancer cells[11] and C‐MYC is widely considered a nucleoprotein in a noncell type‐specific manner,[23] we speculated that PDCD11 and C‐MYC might be colocalized to form a complex in the nucleus of p53‐mutant cancer cells, thereby affecting reported intranuclear C‐MYC‐SKP2 interaction.[7a] We first performed HitPredict analysis[24] and identified C‐MYC as a highly probable binding partner with PDCD11, as confirmed by the results of five independent high‐throughput experiments (Table S1, Supporting Information). This evidence concerns the gene SKP2 and cancer.