Our results parallel the studies of Bhoumik et al. [36] who demonstrated that expression of a dominant-negative of c-Jun (TAM67) or treatment of the melanoma cells with JunD siRNA (which should result in decreased AP-1 activity) attenuated the sensitization of melanoma cells expressing the ATF-2 peptide inhibitor to apoptosis after treatment with anisomycin. The gene discussed is JUN; the disease is melanoma.