Using different RET-dependent breast cancer models, including the Ret/MTB transgenic mouse (Gattelli et al., 2018), we have reported that pharmacological inhibition of RET activity or Ret downregulation, reduces cell proliferation, inflammation and metastatic potential (Boulay et al., 2008; Gattelli et al., 2013, 2018), and that RET-driven tumor outgrowth is accompanied by increased levels of Stat3 and also Stat1 phosphorylation (Gattelli et al., 2013, 2018). The gene discussed is STAT1; the disease is breast cancer.