Specifically, the role of CDKN2A inactivation in allowing escape from tumor senescence has been documented in pediatric LGGs [25, 35], and results from a pediatric LGG xenograft murine model suggests that CDKN2A deletion, in combination with BRAFV600E mutation, is a key molecular change that mediates tumor progression, invasion, and migration [33]. This evidence concerns the gene CDKN2A and neoplasm.