Therefore, we hypothesized that in lung adenocarcinoma, high expression of RACGAP1 leads to aberrant cell cycle regulation, which may include overactivation of cell cycle protein-dependent kinase (CDK) and deletion of CDK inhibitors, which prevents the tumor stem cells from being subjected to normal cell cycle regulation, thus increasing the activity of tumor cells. Here, RACGAP1 is linked to lung adenocarcinoma.