Through NPM-mediated homodimerization, ALK is constitutively activated in ALCL, leading to increased proliferation and tumorigenesis through promitogenic, antiapoptotic, and transforming pathways, particularly STAT3, JUNB, AP-1, MAPKs, and PI3K/mTOR/AKT (6–12). This evidence concerns the gene NPM1 and anaplastic large cell lymphoma.