Mutation-induced activation of the JAK/STAT pathway seems to be a feature of EATL-I as well, but relies on alterations in genes that are distinct from those most frequently involved in EATL-II: in particular, whereas no STAT5B mutations were identified in any of the eight EATL-I tumours tested, recurrent mutations in JAK1 and STAT3 were observed. The gene discussed is SOAT1; the disease is neoplasm.