The results showed that PREX2 knockdown decreased the phosphorylation levels of ERK1/2, MEK1/2 and AKT (Figure 1F), while overexpression of PREX2 catalytic DH-PH domain resulted in elevated phosphorylation of ERK1/2, MEK1/2 and AKT in NSCLC cells (Figure S3D). This evidence concerns the gene MAP2K1 and non-small cell lung carcinoma.