To evaluate the potential role of 12-lipoxygenase (12-LOX) in radiation-induced murine fibrosis, Chung et al. compared the different levels of M2 phenotype biomarkers from primary macrophages cultured in ATII media between wild-type and 12-LOX-deficient mice and found that senescent ATII cells may facilitate macrophage polarization into the preferential M2 type via the 12-LOX dependent pathway in the PF microenvironment [121]. This evidence concerns the gene ALOX12 and fibrosis.