In conclusion, we have identified a high frequency of deletion in the CDKN2A gene in primary melanoma tumors, which supports previous evidence that gene deletion is the major mode of inactivation of CDKN2A and bypass of cell cycle control required for proliferation and progression to metastatic disease in malignant melanoma. Reduced gene dosage at 9p (but not BRAF or NRAS mutation) was associated with histological features predictive of a poorer prognosis. The study also suggests that loss of P14ARF has an additional role in melanoma relapse and possibly also a role for CDKN2B coded by CDKN2B.