In this study, we firstly demonstrated that interaction of RIP with FAK decreased in time-dependent manner in TPL-treated human melanoma cells, whereas that of RIP with Fas/FADD complex increased, suggesting that apoptotic condition induced by TPL triggers the dissociation of RIP from FAK through FAK dephosphorylation and enhances the formation of RIP/Fas complex formation initiating cell death via increase of Fas and FADD expression levels. The gene discussed is PTK2; the disease is melanoma.