Pre-clinical studies utilizing various models of NSCLC suggest that CDKN2A LOF independently contributes to an aggressive tumor phenotype29,30, whereas recent clinical studies in pancreatic adenocarcinoma31, melanoma19, and urothelial carcinoma20 demonstrate an association between CDKN2A alteration and worsened OS and ICB resistance. Here, CDKN2A is linked to neoplasm.