Interestingly, we observed that treating cells with a commercially available STAT5 inhibitor that targets the SH2 domain of STAT5 [30], inhibiting IFNα-stimulated STAT5 tyrosine phosphorylation without affecting STAT3 in human Burkitt’s lymphoma Daudi cells, increased xCT mRNA and protein levels without affecting intracellular ROS levels [31], suggesting that STAT5 could directly affect transcription at the xCT gene locus by acting as a repressor. Here, STAT5A is linked to Burkitt lymphoma.