Melanocytic dysplastic nevi were first described in both patients and their relatives who had one or several cutaneous malignant melanomas. Most of these dysplastic lesions are biologically stable, but some of them have severe histological atypia and can progress further to melanomas. Although several studies have suggested the etiological importance of dysplastic nevi in the development of melanomas, comprehensive reviews of the molecular changes in these dysplastic lesions are still scarce. To remedy this issue, this article analyzes the available molecular information about dysplastic nevi and provides the current state of knowledge regarding the karyotypic abnormalities of the melanoma/dysplastic nevus trait and the involvement of allelic loss, tumor suppressor genes, mismatch repair proteins, microsatellite instability, oncogenes, extracellular matrix proteins, and growth factors in the genesis of these lesions. These studies suggest that although some of these lesions represent "genetic dead-ends," others represent intermediate lesional steps in the melanoma tumorigenesis pathway.