Conclusion: Overall, our results indicate that PREX2 and AHCYL1 promote lung cancer development and reveal a novel regulatory mechanism of PREX2 GEF activity by AHCYL1, which will contribute to the understanding of NSCLC pathogenesis and offer new targets and strategies for the diagnosis and treatment of NSCLC. This evidence concerns the gene AHCYL1 and non-small cell lung carcinoma.