Fraser E et al. have reported that monocytes from patients with IPF displayed increased expression of CD64 (FcγR1), which correlated with the amount of lung fibrosis and an amplified type I interferon response ex vivo, indicating that a primed type I interferon pathway may contribute to driving chronic inflammation and fibrosis [14]. This evidence concerns the gene FCGR1A and idiopathic pulmonary fibrosis.