Analysis of mutation type confirmed that while canonical tumor suppressors such as TP53, CDKN2A, and NOTCH1 frequently harbor premature stop codons, cSCC-associated somatic variants in COL11A1 were primarily missense mutations, suggesting functional consequences at the protein level that might be more nuanced than simple loss-of-function (Fig. 1b). The gene discussed is CDKN2A; the disease is neoplasm.