There were no differences in VEGF-stimulated p-VEGFR2:VEGFR2 or p-ERK1/2:ERK1/2 levels between the endothelial cells from pdgfrβcre-;fakfl/fl or pdgfrβcre+;fakfl/fl mice or between endothelial cells stimulated with PlGF, indicating that the enhanced endothelial cell proliferation in tumours grown in pdgfrβcre+;fakfl/fl mice was due to secondary effects of pericyte FAK-deficiency (Fig. 2g). The gene discussed is MAPK3; the disease is neoplasm.