For somatic copy number alterations, cases with high PLK3 expression not only demonstrated significant amplification peaks for PIK3C2B, PDGFRA, EGFR, and CDK4, which are defined as oncogenic drivers [33,34], but they also showed deletion peaks for tumor-suppressor genes, such as CDKN2A and CDKN2C [35]. The gene discussed is CDKN2A; the disease is neoplasm.