Though no STAT3/STAT5b mutations have been found in alloHSCT recipients with LGL expansions to date, Liang et al. found that a significant subset of such patients showed nuclear expression of phosphorylated STAT3 protein by immunohistochemistry, which has been associated with constitutive activation of the STAT3 pathway in de novo LGLL, even in the absence of somatic mutations [60,190]. This evidence concerns the gene STAT5B and T-cell large granular lymphocyte leukemia.