Cardiac fibrosis is tissue scarring that typically follows a heart attack. Growing evidence suggests that this scarring process is mediated by RGS proteins, multifunctional regulators of cell signaling. To better understand how, researchers examined the effects of RGS4, both on in vitro and in vivo models of heart attack. All models showed elevated levels of RGS4, linking the protein to cardiac fibrosis. Silencing RGS4 through RNA interference proved capable of reducing cardiac fibrosis in vitro and in mice. But when overexpressed, RGS4 could counteract the protective effects of choline, a nutrient found in meat that has been shown to reduce cardiac fibrosis. Further experiments revealed that RGS4 exerts its pro-cardiac fibrosis effects through TGFβ1/Smad and MAPK signaling. Future studies will examine how RGS4 interacts with similar proteins to cause cardiac fibrosis, which could lead to new ways of combating the harmful after-effects of heart attack.