ALK-mediated AKT activation leads to IKK phosphorylation, causing IκB-α degradation and NF-κB nuclear translocation, then NF-κB induces transcription of pro-survival and inflammatory genes, remodel the tumor microenvironment through NF-κB–mediated inflammatory responses, creating a pro-tumorigenic microenvironment that favors disease progression (33). The gene discussed is AKT1; the disease is neoplasm.