Cellular therapy to replace lost myocardial mass with new, contractile myocardium has the potential to revolutionize the treatment of myocardial infarction and heart failure. Studies have shown small but consistent improvements in mechanical function, largely independent of the cell type chosen. The reasons for this lack of specificity are presently unknown. In the current issue of Circulation, Wall et al 1 present computational models that suggest that the injection of passive materials alone may improve ejection fraction and reduce wall stress in the ventricle. The present study raises the possibility that some cellular therapies contribute to increased heart function purely through a passive mechanism rather than through active contraction associated with the addition of new myocytes. Because materials lack many of the uncertainties associated with cellular therapies (eg, mode of delivery, homing, immune rejection, arrhythmias), and because they can be engineered to have a number of inherent advantages (eg, uniformity, reliability, greater safety, reduced cost), one conclusion of the current finding is that biomaterials alone may be important for future cardiac therapy. Article p 2627 Given the results of this study by Wall and colleagues,1 it is also clear that passive contribution must be separated from active contribution to evaluate the efficacy of any cell therapy approach. Passive contribution can result from replacing a stiff material, such as an infarct, with a more compliant material. Completely replacing the infarcted tissue with a compliant scaffold can accomplish this task. Matsubayashi and colleagues 2 demonstrated that passive properties can improve global heart function by seeding a synthetic scaffold with smooth-muscle cells before implantation in a fullthickness ventricular defect model. The smooth-muscle cells, which are unlikely to contribute contractile function, increased elastic tissue formation and likely increased the compliance of the scaffold. Skeletal myoblasts, which have been employed in clinical trials, are also unlikely to contract in synchrony with the normal myocardium. These cells do not make connexins, the building blocks of gap junctions, and are therefore unlikely to make electrical connections with the native myocardium.3 Several reports, however, have documented improved mechanical function with these cells. 4 Such improvement is likely the result of improved passive function and not the addition of contractile mass. The present study suggests that this improvement could also result from the addition of an inert biomaterial to the infarcted region. Whereas skeletal myoblasts leave the heart susceptible to arrhythmias, 5 a biomaterial can be chosen to provide electri