IR expresses higher levels of metallothionein antioxidant genes, Mt1 and Mt2 (10), which can modulate injury-induced oxidative stress and fibrosis in the heart (42), as well as neutrophil and monocyte/macrophage chemoattractants and activators including CCL7, CCL2, CXCL5, and MIF (Fig. 1, E and G, and table S1) (10), suggesting that IR is a proinflammatory CF population, potentially related to those reported previously (43). Here, MIF is linked to cystic fibrosis.