FERMT2 and lung adenocarcinoma: Thus, it is likely to be that kindlin-2, through its interactions with ECM adhesion receptors such as integrins45,46, actin cytoskeletal regulatory proteins such as ILK30,47, paxillin48, Arp2/349, and MLCK37, and metabolic enzymes such as PYCR1 (the current study), promotes ECM adhesion, actin cytoskeletal contraction, cell survival, proliferation, metabolic reprograming, and collagen matrix deposition in both lung adenocarcinoma cells and associated fibroblasts, which collectively contribute to the progression of lung adenocarcinoma.