One potential explanation for the activity of dovitinib plus fulvestrant regardless of FGF pathway amplification status is that, as a multitargeted tyrosine kinase inhibitor, dovitinib targeted other pathways [36], such as signaling through vascular endothelial growth factor receptor or c-Kit, which are overexpressed in 10% to 11% and 11% to 17% of breast cancers, respectively [39, 40]. Here, KIT is linked to breast carcinoma.