Finally, SNVs in the FAM13A gene have been associated with an increased risk of COPD and IPF [8]; the most critical part of the FAM13A protein is its N-terminal extension containing the Rho-GAP domain involved in lung endothelial barrier function, which is often deregulated in lung diseases [9]. Here, ARHGAP1 is linked to idiopathic pulmonary fibrosis.