The marked increase of the kindlin-2 and PYCR1 levels in lung adenocarcinoma, together with the molecular and cellular studies showing that kindlin-2 interacts with PYCR1 and promotes PYCR1 and proline levels and cell proliferation, beg the question as to whether kindlin-2 is involved in promoting lung tumorigenesis in vivo. This evidence concerns the gene FERMT2 and lung adenocarcinoma.