In addition, and in contrast to IKKα loss, knockdown of the noncanonical NF-κB p52 subunit in the H1299 and A549 NSCLC lines reduced their tumor xenograft burdens in immune-compromised NSG mice, indicating that IKKα’s NSCLC tumor suppressor activity is independent of its unique function to activate the NF-κB noncanonical signaling pathway. Here, NFKB2 is linked to neoplasm.