The activation of oncogenic driver signals, such as MYC, RAS/ERK, PI3K/AKT, and NF-κB, as well as the dysfunction/loss of pivotal tumor suppressors, such as TP53 or CDKN2C, cooperatively and sometimes compensatively promote the disease progression, the aggressiveness, and treatment-resistant phenotype of tumor cells [3,6,10,11,12,13,14,15]. The gene discussed is NFKB1; the disease is neoplasm.