Additional genomic alterations, such as more extensive p3 deletions, inactivation of Trp53 and/or Cdkn2a or overexpression of c-Myc, may synergize with the genomic perturbations in the BPS-TA and BPS-Cre models to induce tumor formation, and hypotheses such as these may be addressed in future studies. The gene discussed is CDKN2A; the disease is neoplasm.