Regarding the link between Notch or Hippo signaling and CDKN1C, prior studies in non‐transformed human mammary cells [53] and murine lymphangiogenesis models [54] identified a role for YAP1 in downregulating CDKN1C, and in human hepatocellular carcinoma primary tumors and cell lines demonstrated a strong inverse relationship between HES1 protein and CDKN1C mRNA levels, with HES1 loss‐of‐function or P57 (the protein name for CDKN1C gene) gain‐of‐function inducing a senescence phenotype [41]. This evidence concerns the gene CDKN1C and hepatocellular carcinoma.