The equal sensitivity of WT mice and IL-4−/− mice pulmonary fibrosis upon WTI argues against a critical role of IL4 in this process that might be explained be potential compensatory effects of the related cytokine IL-13: IL-13 also binds to receptors shared with IL-4, thereby mediating pro-fibrotic actions [227, 228]. This evidence concerns the gene IL4 and pulmonary fibrosis.