However, pathogenesis of LGL leukemia is not driven only by chronic antigen and proinflammatory cytokine stimulation, but also by constitutive activation of Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway and resistance to Fas/Fas-ligand (Fas-L)-mediated apoptosis [1,2,38]. Here, FASLG is linked to T-cell large granular lymphocyte leukemia.