Therefore, IGF-II may be repressing the expression of the TIMP repressor in addition to MMP3 transcripts, while facilitating the type and scale of extracellular delivery of pro-fibrotic factors (preferentially switching from the more specific inhibitor TIMP4 in NL to the broader inhibitor TIMP1 in IPF and SSc, based on the sheer magnitude of secretion in IPF and SSc compared to NL, Fig 4). Here, TIMP4 is linked to idiopathic pulmonary fibrosis.