For example, the pathways reported potentially to mediate CD109′s tumorigenic effect in lung adenocarcinoma include JAK-SAT [19], Hippo-YAP [37], and EGFR-AKT-mTOR [38], but their relative significance and potential cross-talk in mediating CD109 action in lung adenocarcinoma are poorly understood. This evidence concerns the gene MTOR and lung adenocarcinoma.