Among the survival signalling pathways, the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway has been associated with LGL transformation.26 Most recently, the role of STAT family genes (STAT3 and STAT5b) in the pathogenesis of T-LGL leukemia has been emphasized.44 Activating somatic mutations in STAT3 were found in up to 40% of T-LGL leukemia patients and it has been suggested that mutational analysis of STAT3 might distinguish true T-LGL leukemia cases from clonally skewed reactive processes.11, 45, 46. The gene discussed is SOAT1; the disease is T-cell large granular lymphocyte leukemia.