On the other end, in its soluble form, decorin is an endogenous ligand to TLR2 and TLR4 and can activate the p38 MAPK and ERK pathways, leading to pro-inflammatory signaling; it may also promote lung fibrosis when degraded by cathepsin-S because fragmentation disrupts its anti-fibrotic capabilities [91,92,93]. This evidence concerns the gene TLR2 and pulmonary fibrosis.