For instance, IL-6-induced STAT3 activation can promote T helper 17 (Th17) cell differentiation by positively regulating the transcription factor RORγt as well as IL-17 expression, whereas IL-2-mediated STAT5 activation disrupts Th17 cell development by constraining IL-17 expression.34 Furthermore, constitutive STAT5 activation is dominant over constitutively active STAT3 in certain types of breast cancer cells and antagonizes the positive regulation of STAT3 upon protein BCL6, which is a critical factor in mammary tumorigenesis.35, 36. This evidence concerns the gene STAT5A and breast carcinoma.