PTPN11 and pulmonary fibrosis: Given our previously published observations that SHP2 overexpression attenuates fibrotic responses both in vivo and in vitro in experimental models of pulmonary fibrosis [12], as well as the fact that: (1) SHP2 also localizes within mitochondrial space and (2) the cardinal role of mitochondrial homeostasis of lung structural cells in lung fibrosis [13], we focused on the role of SHP2 as a regulator of mitochondrial metabolism in primary MLFs derived from mice carrying a conditional knock-in mutation (D61G/+) that renders the SHP2 catalytic domain constitutively active.