TGF-β1 is an essential molecule leading to LF fibrosis, and TGF-β1 exerts its fibrosis-stimulating effects via the Smad2/3, PI3K/Akt, β-catenin, and ERK1/2 signaling pathways.[2,30,73] It is feasible to inhibit LF fibrosis by modulating the concentration and potency of TGF-β1 in the serum and LF tissues. This evidence concerns the gene SMAD2 and Lassa fever.