AKT1 and neoplasm: Indeed, recombinant PDGF-C (rPDGF-C) treatment of fibroblasts but not ER+ tumor cells promoted PDGFRα, AKT, ERK and S6 phosphorylation, which was suppressed by the PDGFRα inhibitor imatinib (Fig. 5b), and, consistent with previous reports22–24, fibroblast proliferation and migration increased following rPDGF-C treatment (Fig. 5c and Extended Data Fig. 8b,c).