CDKN2A and neoplasm: Mice that are null for p19 (but not for p16), generated by deleting exon E1β,32 develop tumours similar to those observed in p16 and p19 double-null mice, although a lack of p19 in association with Tax oncogene expression has been implicated in osteosarcoma development.33 Wild-type keratinocytes of the oral epithelia express p16 at higher levels than skin keratinocytes, suggesting that p16 loss could be important in oral tumourigenesis.