Furthermore, the activation of PI3K/AKT, MEK/ERK, and SAPK/JNK downstream pathways of epidermal growth factor receptor (EGFR) can upregulate LOX expression, while the traditional anti-fibrosis drug silibinin represses EMT and ECM remodeling in NSCLC by blocking the EGFR/LOX pathway, thus inhibiting NSCLC invasion and migration [39]. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.