The tumor-promoting effects of AHCYL1 in NSCLC appear to rely heavily on its partnership with PREX2, as AHCYL1 knockdown specifically disrupts PREX2 GEF related signaling pathways in NSCLC but not in normal lung epithelia cell NL20 with low expression of PREX2. This evidence concerns the gene PREX2 and non-small cell lung carcinoma.