Thus, the increased expression of kindlin-2 detected in lung adenocarcinoma is functionally significant, in that it not only functions in intracellular signaling but also promotes collagen matrix formation and consequently ECM stiffening, which in turn promotes the formation of the kindlin-2–PYCR1 complex, proline synthesis, and cell proliferation. Here, PYCR1 is linked to lung adenocarcinoma.