This was shown to be independent of gp130 expression and to be due to differential IL-6 signaling in these two fibroblast populations: in normal lung fibroblasts, IL-6 induced sustained STAT3 signaling leading to increased expression of the Cyclin Dependent Kinase Inhibitor (CDKI) p19INK4D; however, in IPF lung fibroblasts, IL-6 induced sustained SHP-2/ERK MAPK signaling leading to the decreased expression of the CDKI p27Kip1, increased Cyclin D1 activation, and enhanced proliferation (Knight et al., 2003). Here, IL6ST is linked to idiopathic pulmonary fibrosis.