Our functional and mechanistic studies together lead us to a tentative hypothetical model (Figure 7C) by which we propose that ARMC4 inhibits NF-κB DNA binding and transactivation abilities downregulate the expression of NF-κB target genes, thereby inhibiting cell proliferation, anchorage-independent growth, migration, and tumor growth in NSG mice. The gene discussed is NFKB1; the disease is neoplasm.