Most likely, HDM2 occupies the C‐MYC‐binding domain on PDCD11 to deactivate the PDCD11‐C‐MYC axis and instead facilitate the degradation of the p53 tumor suppressor.[11] Upon this hypothesis is solidly confirmed in the future, the undeveloped PDCD11 antagonists would be promising therapeutic drugs against a broad spectrum of human cancers by hindering the formation of either the PDCD11‐HDM2 or PDCD11‐C‐MYC complex. Here, MYC is linked to cancer.