Alternative but not mutually exclusive mechanisms recently reported include disruption of Stat5a/b phosphorylation during breast cancer progression through upregulation of the Jak2 tyrosine phosphatase, PTP1B [43], or inhibitory signaling to Stat5 by the truncated ERBB2 isoform, p100-t-ERBB2 [45]. The gene discussed is STAT5A; the disease is breast cancer.