In conclusion, our study demonstrated that isoform C of WT1 is conservely expressed in lung cancer patients and indicates that the down-regulation of WT1 mediated by siRNA could inhibit the growth of lung cancer cells effectively, arrested the cell cycle at the G1 phase, and may enhance the lung cancer cell sensitivity to DDP treatment via the PI3K/AKT signaling pathway. Here, WT1 is linked to lung carcinoma.