Treatment of cell line and genetically modified mouse models of triple-negative breast cancers (TNBCs) with the allosteric MEK inhibitor Selumetinib rewired the tumor cell kinome to activate multiple tyrosine kinases such as PDGFRβ, AXL (AXL receptor tyrosine kinase), VEGFR2, and DDR1 (discoidin domain receptor tyrosine kinase 1) (2). Here, DDR1 is linked to neoplasm.