Two mutually exclusive mechanisms independent of ALK activation lead to the constitutive activation of STAT3 in ALK- ALCL: (1) oncogenic point mutations in JAK1 and/or STAT3 (~20% of cases), and (2) oncogenic fusion genes displaying concomitant transcriptional and kinase activities capable of sustaining the ALCL phenotype via STAT3, namely NFKB2-ROS1, NCOR2-ROS1, NFKB2-TYK2, and PABPC4-TYK2 fusions (rare cases) [66] (Figure 9A). This evidence concerns the gene JAK1 and anaplastic large cell lymphoma.