The SMs induce the ubiquitination and degradation of two fungible IAPs, cIAP1 and cIAP2, altering TNF-α signaling pathways in cancer cells away from survival and inflammatory MAPK and classical NF-κB and AP-1 signaling toward the induction of apoptotic (RIPK1 and caspase-8 dependent) or necroptotic cell death (RIPK1, RIPK3, and mixed-lineage kinase-like (MLKL) dependent) pathways (Fig. 1)4. Here, NFKB1 is linked to cancer.