These include caspase-3-mediated secretion of pro-survival factors (e.g., prostaglandin E2) that promote enrichment of tumor repopulating cells [37,38,39,40,41], and caspase-3/DNase-mediated accumulation of genome instability (e.g., DNA double-strand breaks) that trigger activation of transcription factors such as NF-κB and STAT3 that drive tumor growth [42,43]. Here, NFKB1 is linked to neoplasm.