In mice, small-molecule inhibition of FAK prevented bleomycin-induced lung fibrosis (109), while ATII-specific deletion of FAK following bleomycin-induced fibrosis resulted in ECM alterations, fibroblast activation, and inhibition of ATII cell apoptosis, suggesting a complex signaling dynamic between epithelial cells and fibroblasts (107). The gene discussed is PTK2; the disease is pulmonary fibrosis.