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. This evidence concerns the gene JAK1 and neoplasm.