Indeed, in BIA-ALCL, recurrent JAK1 and STAT3 mutations leading to activation of the JAK/STAT pathway are frequently demonstrated and STAT3 phosphorylation is uniformly demonstrated in contrast to the more heterogeneous STAT3 phosphorylation seen in ALK-negative sALCL [5,7,8,10]. The gene discussed is JAK1; the disease is anaplastic large cell lymphoma.