One of the well‐known features of CS is the over‐activation of the p16ink4a and/or p53‐p21Cip1/Waf1 pathways, which inhibit cyclin‐dependent kinases to block cell cycle progression (Hernandez‐Segura et al., 2018; Purvis et al., 2012; Sherr et al., 2016). The gene discussed is CDKN1A; the disease is Cowden syndrome 1.