While we have utilized vMSCs to both understand and exploit the physiological role of MSC-CM fusion, induction of fusion of another stem cell, progenitor, or even mature cell types may augment our ability to repopulate and repair the damaged myocardium [59, [73] [74] [75] [76] [77] [78] [79] . In the case of mature or progenitor cell transplantation, the induction of fusion may be less beneficial from a differentiation standpoint and more beneficial from an engraftment or retention standpoint. One of the primary challenges for stem cell delivery is the ∼90% cell loss after transplantation [80] [81] [82] that has prompted the development of new methods to deliver and maintain cells in the heart [48, 83, 84] . This is particularly problematic for cardiac therapy as the heart is mechanically active, rapidly flushing cells from the intended target region. If stem cells transiently express a viral fusogen, they might rapidly adhere and so be maintained long term in the heart. The added advantage of pH sensitive fusogens, such as VSV-G, is the ability to control activity such that cells only fuse at pH lower than 6.5. This has major implications for inducing temporally (the window during ischemia) and spatially (the ischemic region) regulated fusion in vivo. In fact, vMSCs delivered to the heart were found in the patch and in damaged myocardium fused with mouse cells. The ability for VSV-G to induce fusion in the patch may be due to close proximity to the ischemic region, causing the environment to be more acidic or by the remodeling of the collagen patch [48] . Collagen remodeling has been shown to occur via MSC secretion of matrix metalloproteinases (matrixins), serine proteases, and cysteine proteases [85] . While matrixins are active at neutral pH, serine and cysteine proteases are active at acidic pH, indirectly demonstrating cells are able to make the microenvironment acidic [86] . Taken together, the induction of cell fusion in the heart could exert functional benefit via multiple mechanisms.