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Graphical summary of the molecular mechanism of the tumor-suppressor function of STAT1-SOCS1. In the presence of STAT1, JAK2 activation is normally regulated by SOCS1, which is transcriptionally induced by STAT1. In MECs that have downregulated STAT1 or are unable to upregulate SOCS1, persistent JAK2 activation results in unopposed STAT3/5A/5B activation, promotes survival of MECs, and drives development of ERα+ mammary tumors. See Discussion section for details
