Additionally, prolonged exposure to HGF expedites the development of clones that are resistant to EGFR-TKIs.[52] When coupled with gefitinib, NCTD may prevent EGFR-mutant lung cancer cells from developing resistance to EGFR-TKIs caused by endogenous and exogenous HGF by blocking the phosphorylation of Met, and subsequently obstructing the PI3K/Akt pathway. Here, AKT1 is linked to lung carcinoma.