Cardiac fibrosis, or scarring of heart tissue, is a common finding in many disorders of the heart, including myocardial infarction, hypertension, and cardiac hypertrophy. A key step in this form of scarring is the transformation of fibroblasts, cells that provide structural, electrical, and chemical support into myofibroblasts, more muscle-like cells expressed only in stressed or failing hearts. A new review explores the important role played by noncoding RNAs in this transformation. Noncoding RNAs, studies are showing, regulate fibrotic scarring through the TGF-β and WNT signaling pathways. TGF-β signaling participates in a variety of heart-related processes, including cardiac repair, hypertrophy, fibrotic remodeling, and fibroblast activation. WNT signaling, meanwhile, is implicated in the pathogenesis of many diseases. Crosstalk between the TGF-β and WNT pathways could be responsible for the transcription of genes that promote fibrosis. Understanding how noncoding RNAs orchestrate the biochemical processes that lead to scarring could provide new avenues for preventing and treating cardiac fibrosis.