The possible reasons might include that (a) based on the correlation of GBP1 with EGFR mutation, GBP1 might lead to autophosphorylation of receptor tyrosine kinase via activating EGFR, initiating a cascade of downstream signaling pathway, and further resulting in cellular proliferation, differentiation, and survival of lung adenocarcinoma. This evidence concerns the gene EGFR and lung adenocarcinoma.