The failure of Simtuzumab to modulate the course of disease in IPF patients motivated us to examine more closely how LOXL2-mediated collagen crosslinking impacted the synthetic and functional properties of primary normal and IPF lung fibroblasts both in vitro as well as in a humanized SCID model of IPF. The gene discussed is LOXL2; the disease is idiopathic pulmonary fibrosis.