Specifically, integrin β3 is able to recruit KRAS and RalB to the cell membrane in an unliganded state, leading to the activation of TBK1 and NF-κB, thus driving tumor stemness and resistance to EGFR-TKI in NSCLC [14].Therefore, a full understanding of the molecular mechanisms of integrin β3 in drug resistance would be helpful to directly design specific targeting strategies. This evidence concerns the gene KRAS and non-small cell lung carcinoma.