In the tumor context, c-FLIP acts as a drug resistance factor able to suppress cytokine- and chemotherapy-induced apoptosis by interacting with the death signaling complex downstream of tumor necrosis factor (TNF)-α receptors, Fas (CD95), and TNF-related apoptosis inducing ligand (TRAIL) receptors 1 (DR4) and 2 (DR5) (42). Here, FAS is linked to neoplasm.