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The use of immune checkpoint inhibitors has markedly improved the survival outcomes of many patients with solid tumors. However, in multiple myeloma (MM), the use of such inhibitors has failed to achieve survival benefit. We previously showed that oncolytic herpes simplex virus 1 (oHSV-1) can effectively infect MM cells and induce apoptosis through the receptors for oHSV-1, NECTIN-1 and HVEM (herpes virus entry mediator). HVEM, a member of the TNF receptor superfamily (TNFRSF14), is an immune checkpoint present on T cells, B cells, NK cells and macrophages. Depending on HVEM's interaction with its major inhibitory ligand, B- and T-lymphocyte attenuator (BTLA) or its major activating ligand, tumor necrosis factor superfamily member 14 (TNFSF14, LIGHT), it is pivotal in downmodulating or stimulating the immune cells. Accordingly, targeting HVEM to block its interaction with BTLA is an area of therapeutic interest.