In support of this concept, a recent study by Chen et al. explored the contribution of TGFβ and IL-11 signaling in a mouse model of senescence-associated lung fibrosis due to Bmi-1 deficiency and showed that TGFβ and IL-11 were both highly secreted by senescent lung fibroblasts and epithelial cells. The gene discussed is IL11; the disease is pulmonary fibrosis.