BCL2 and idiopathic pulmonary fibrosis: The mitochondria from airspace macrophages isolated from patients with IPF have 4-fold higher expression of BCL-2 compared with controls, while Bcl-2 deletion in macrophages or inhibition with ABT-199 has been shown to prevent fibrosis development after both bleomycin- and asbestos-induced fibrosis and accelerate spontaneous resolution in mice after single-dose bleomycin (43).