Uchida et al. (2012) described another approach at retargeting oHSV by eliminating the natural receptor-binding activities of glycoprotein D; introducing single-chain antibodies specific for EGFR, which is overexpressed in many gliomas; and adding entry-accelerating mutations to glycoprotein B into a detargeted mutant form of glycoprotein D. The novel virus entered through EGFR and achieved infection similarly to wild-type virus while prolonging survival in mice with orthotopic primary human GBM xenografts. The gene discussed is ACKR1; the disease is infection.