Therefore, we sought to determine if α-SMA+ fibrotic fibroblasts express antiapoptotic BCL-2 family members in human PF-ILDs, IPF, and silicosis (Supplemental Table 1; supplemental material available online with this article; https://doi.org/10.1172/jci.insight.163762DS1), by co-immunostaining human tissue from healthy donors, IPF, and silicosis for α-SMA and antiapoptotic BCL-2 family members. The gene discussed is ACTA1; the disease is idiopathic pulmonary fibrosis.