Therefore, we established four cell lines from two parental MET-amplified lung carcinoma cell lines, which have acquired resistance to crizotinib and revealed various possible molecular mechanisms of resistance from PAI-1 overexpression, involvement of MAPK pathway activation and acquisition of EMT features to possible therapeutic strategies to address the resistance using combination therapy with various therapeutic agents such as tiplaxtinin and trametinib (Table 1). This evidence concerns the gene SERPINE1 and lung carcinoma.