Although the role of IKKα in promoting cancer has been well established in the context of lung cancer driven by Kras-activating mutations, it may have tumor-suppressing activity: in a KrasG12D-driven spontaneous mouse model of NSCLC, lung-specific Ikkα deletion induced by intratracheally injected adenovirus-Cre recombinase promoted NSCLC initiation and growth by elevating the expression of inflammatory cytokines and chemokines, including NF-κB targets20. Here, KRAS is linked to neoplasm.