The above data support the hypothesis that miR-128 may have a function in NSCLC carcinogenesis, partly through the modulation of lymphangiogenesis and angiogenesis by targeting VEGF-C and concurrently blocking ERK, protein kinase B (PKB), also known as Akt, and p38 signal transduction pathways. Here, AKT1 is linked to non-small cell lung carcinoma.