We report that (i) it is possible to modify HSV tropism by inserting in gH the 20-aa short GCN4 peptide, (ii) the gH-mediated retargeting can be combined with the gD-mediated retargeting to HER2, as the double-retargeted HSV can use the GCN4 receptor and the HER2 receptor as alternative portals of entry to infect different sets of cells; (iii) the alternative usage of two receptors has enabled the development of a non-cancer cell line to grow retargeted oncolytic HSVs. Here, ERBB2 is linked to cancer.