Using these vectors, we found that overexpression of EGFR and PDGFRα in hiPSCs, which are resistant to HCMV infection,43 rendered these cells permissive to TB40/E infection (Figure 5F), supporting the idea that both EGFR and PDGFRα are important mediators of HCMV infection. The gene discussed is EGFR; the disease is cytomegalovirus infection.