Coimmunostaining showed that ACP5 was almost undetectable in the lung sections from control subjects, while IPF patient-derived lung sections were characterized by a large amount of lung myofibroblast aggregation, manifesting as high levels of ACP5 revealed by costaining for ACP5 with α-SMA (Fig. 1f). Here, ACP5 is linked to idiopathic pulmonary fibrosis.