The adult heart is incapable of healing after heart attacks or other insults to the heart muscle. Instead, scar tissue typically forms around the damaged area from proliferating cardiac fibroblasts, which outnumber cardiac myocytes by about two to one. Two groups have demonstrated a way to shift the balance toward myocytes by transfecting cardiac fibroblasts in situ with a set of transcription factors that direct heart development. And more incredibly, in a mouse model of heart attack, the induced cardiomyocytes improve cardiac function, despite the fact that only a few percent of cells in the area are transfected. The factors involved (GATA4, MEF2C, TBX5 and HAND2) had previously been shown to transdifferentiate fibroblasts to myocytes in vitro. Now by injecting retroviruses carrying three or four of the factors in or around the area of damage, fibroblasts take on the appearance and the expression patterns of myocytes. As the recovery seems out of line with the efficiency of transfection, other elements, such as growth factors or cytokines, perhaps attracted to the site, may be involved. (Nature 485, 593–598, 2012; Nature 485, 599–604, 2012)