In a model of alternative activation of NF-kB in ALCL revealed by CRISPR screening, Wang et al found that in NF-kB-inducing kinase (NIK)-positive ALK- ALCL cells, common JAK/STAT3 mutations promote transcriptional activity of STAT3 which directly regulates NFKB2 and CD30 expression [108]. This evidence concerns the gene NFKB1 and anaplastic large cell lymphoma.