Furthermore, mice lacking CD69 develop an exacerbated form of autoimmune disease, thus indicating a pivotal regulatory role for CD69 in modulating T lymphocyte differentiation through the activation of the Jak-3 signal transducer and activator of the transcription (Stat)-5 signalling pathway, which inhibits T-helper 17 cell differentiation [45]. Here, JAK3 is linked to autoimmune disease.