In a recent study published in Cell, Zhang, Thai et al. conducted a high-throughput drug screen on iPSC-derived cardiac fibroblasts, identifying artesunate as a potent antifibrotic compound.1 Mechanistically, artesunate interferes with the formation of the TLR4/MD2-signaling complex to suppress profibrotic gene expression, positioning it as a promising candidate for drug repurposing in heart failure. Here, TLR4 is linked to heart failure.