We previously demonstrated that oHSV infection induces IGF2 secretion, activating IGF1R signaling and reshaping the tumor immune microenvironment (TIME) by recruiting immunosuppressive myeloid cells (e.g. mMDSCs, gMDSCs).8 Herein, we extend these findings by showing that oHSV triggers IGF2/IGF1R activation not only in infected tumor cells but also in neighboring uninfected cells, promoting tumor regrowth and therapeutic resistance. The gene discussed is IGF1R; the disease is neoplasm.