In agreement with these data, we provide evidence that overexpression of SRSF1 in cellular models derived from human lung adenocarcinoma leads to a more aggressive phenotype with activation of p42/44MAPK and AKT signaling pathways, increased colony formation in soft agar, epithelial to mesenchymal transition and resistance to carboplatin and paclitaxel. The gene discussed is AKT1; the disease is lung adenocarcinoma.