CDKN2A and neoplasm: Recent genetic characterization of ALM patient tumor tissue has identified cyclin-dependent kinase 4 (CDK4)-pathway (e.g., CDK4 amplification, CDK6 amplification, CCND1 amplification, P16INK4A loss) alterations in 53–82% of ALM cases [2, 7], with CDK4 amplification and P16INK4A loss each independently serving as predictors of shorter patient overall survival.