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Mesothelioma is a cancer marked by a distinct pattern of mutations unlike most other solid tumors. Direct mutation of genes such as p53 or ras family members may be rare and distinctly different from the well-characterized spectrum of mutations seen in the more common epithelial malignancies such as lung or bladder cancer. This may be partially a result of the unique contributions of asbestos and SV40 infection as co-carcinogens in mesothelioma. Nonetheless, aberrations of the regulatory genes expressed at the 9p21 locus ( p16 ^INK4a, p14 ^ARF) and chromosome 22 ( NF2 ) are clearly among the highest frequencies observed in human cancers. In addition, recent investigations into epigenetic inactivation following SV40 infection may yield new gene targets such as RASSF1A that are inactivated by pathways that have not been sufficiently explored in the past. The presence of normal DNA within mesothelioma tumors is likely not to be equated with the presence of a normal protein phenotype in the future. This holds the promise of potentially reversible epigenetic or infectious molecular defects accounting for much of the transformed phenotype in mesothelioma, and the distinct possibility of novel therapeutic modalities that may reverse these acquired defects in gene expression patterns.