Following the binding of TNF to its death receptor TNFR1, and subsequent recruitment of the TNF-associated death domain (TRADD) adapter protein, two events can occur: (i) activation of pro-inflammatory and potentially pro-tumor survival pathways through NF-κB, JNK and p38 or (ii) induction of apoptotic cell death via recruitment of Fas-associated death domain (FADD) and caspase-8 activation, culminating in the activation of caspase-3 [20, 21]. The gene discussed is CASP3; the disease is neoplasm.