While we observed no association between overall STAT3 mutation and pY-STAT3 phosphorylation, pY-STAT3 phosphorylation was most elevated in PTCL patients with combined CD30+ tumor phenotype and mutations in either STAT3 or JAK1 representing primarily ALK− ALCLs and suggesting heterogenous mechanisms of STAT3 activation. The gene discussed is ALK; the disease is mature T-cell and NK-cell non-Hodgkin lymphoma.