The lack of ICP6 confers virus selectivity towards mitotic cells or cells with a p16INK4a deletion [203], suggesting a potential benefit in the treatment of mesothelioma with a loss of function of CDKN2A. Deletion of ICP34.5, a viral homologue of GADD34, markedly reduces the neurovirulence of the construct but inhibits viral protein synthesis [204], which consequently blunts viral replication and therapeutic efficacy. This evidence concerns the gene CDKN2A and mesothelioma.