STAT3 and T-cell large granular lymphocyte leukemia: Remarkably, recurrent gain-of-function somatic mutations have recently been discovered in the Src homology (SH) 2 domain of STAT3 in 27–40% of patients with T-LGL leukemia and 30% of NK-LGL patients, which increase the gene’s transcriptional activity, leading to constitutive STAT3 activation and gene dysregulation downstream of STAT3 [9,10].