Several studies show that, whereas the complete knockouts of PDGF-B or PDGFRβ are lethal during late embryonic development or at birth [41], [42], the exchange of the intracellular domain of PDGFRβ for that of PDGFRα produces viable mice but with a severe deficit in retinal pericytes and who subsequently develop retinopathy [43]. The gene discussed is PDGFB; the disease is retinal disorder.