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. This evidence concerns the gene CNTN2 and osteosarcoma.