Recently, a new fusion of ALK with TRAF1 was found in patients with ALCL, which had an aggressive clinical course because the fusion leads to the constitutive activation of NFκB and acquisition of multiple genetic defects such as mutant TP53, the losses of PT53 and PRDM1/Blimp1 [55]. This evidence concerns the gene PRDM1 and anaplastic large cell lymphoma.