Fibrosis, defined as the pathologic accumulation of extracellular matrix, is the final outcome of several common chronic inflammatory, immune-mediated, and metabolic diseases and accounts for up to 45% of all deaths in the industrialized world.1 The approval of pirfenidone and nintedanib for the treatment of idiopathic pulmonary fibrosis (IPF), a rapidly progressive and fatal fibrotic condition, represented a defining moment for the development of antifibrotic therapeutic agents.2,3 However, although these agents slow the decline in lung function, they do not halt disease progression, so IPF continues to represent a disease of high unmet clinical need. In this issue of the . . .