In general, CDKN2A is frequently inactivated in human malignant tumors by its gene aberrations, such as deletions or mutations [9, 10], but diffuse p16 expression was also reported in various human malignancies, e.g., high-grade breast and lung cancers and/or undifferentiated pleomorphic sarcoma without significant association with its gene alteration status [9, 11]. Here, CDKN2A is linked to lung cancer.