Increasing the frequency of MSC-CM cell fusion will aid in the study of cell fusion in vitro and may improve the therapeutic benefit of MSCs in vivo. One way that the therapeutic benefit may be improved is via induction of programming of MSCs to a cardiomyocyte fate. Differentiation of MSCs into CMs can be initiated in vitro via soluble factors including 5-azacytidine [62] [63] [64] or with exposure to insoluble factors including laminin [65] . However, functional differentiation of MSCs to cardiomyocytes has only been accomplished to date via cell fusion with mature cardiomyocytes. This result has been demonstrated in vitro [66] and in vivo wherein MSC-CM fusion products take on a cardiomyocyte morphology, express cardiomyocyte markers, and couple to adjacent cardiomyocytes [60] . Here we find that when MSC-CM fusion is induced with viral fusogens, the CM fusion partner is dominant in that the majority of fusion products (regardless of medium type) adopt a CM-like morphology and maintain expression of MF20 and lose CD105. These data further support the exciting possibility that induction of fusion with viral fusogens could enhance MSC programming to a CM fate in vivo. Of note, the CMs utilized here are HL-1 CMs. This cell line was used to enable largescale and long-term studies. However, the heterogeneity and immortal nature of these cells may account for the seeming dominance of the CM phenotype and future studies will utilize primary fetal cardiomyocytes or induced pluripotent stem cell-derived cardiomyocytes.