CDKN2A and neoplasm: Recently, it was shown with the use of knockout mice for Cdkn2a/2b and/or Pten that DNA double-stranded breaks cooperate with the loss of Ink4 and Arf (protein products from Cdkn2a/2b after alternative splicing) tumor suppressors to generate glioblastomas with frequent c-Met amplification (Camacho et al., 2014).