Blocking the cFLIP/calmodulin interaction could also be more effective than targeting the interactions between calmodulin and other DISC components (such as Fas, for instance), especially in the case of tumor cells that become resistant to Fas-stimulation in response to chemotherapy, a mechanism which has been linked with increased recruitment of cFLIP to the DISC [9, 22]. This evidence concerns the gene FAS and neoplasm.