While RET activity has not been directly identified as a pro-tumorigenic kinase in TNBC, multiple studies demonstrate that MKIs can target RET to inhibit TNBC growth and proliferation in vitro and in vivo. For example, vandetanib can target RET, as well as, vascular endothelial growth factor receptor 2 (VEGFR-2) and epidermal growth factor receptor (EGFR), but exhibits potent anti-tumor effects against TNBC patient-derived xenografts with RET hyperactivity (163), suggesting RET inhibition as a novel treatment modality in TNBC patients. This evidence concerns the gene RET and neoplasm.