Moreover, Timp1 KO mice exposed to MWCNTs as summarized in Table 2 had reduced lung fibrosis, suppressed myofibroblast differentiation, and lower activation of extracellular signal-regulated kinase (ERK) signaling, indicating that TIMP1 plays a pro-fibrotic role in the progression of MWCNT-induced lung fibrosis through activation of the intracellular ERK pathway [112]. Here, TIMP1 is linked to pulmonary fibrosis.