To elucidate the mechanisms underlying the KLF17 inhibition of uPA in invasion of lung adenocarcinoma, we analyzed whether or not KLF17 participated in the Src, p38/MAPK, JNK, AKT or ERK pathways, and the results demonstrated that the phosphorylation of Src and p38/MAPK was significantly decreased in the KLF17-overexpression groups (pLV.O-KLF17) compared to the control groups (pLV.O-NC) or parental groups in A549 and H322 cells (Figure 5A–5D, p < 0.05). Here, AKT1 is linked to lung adenocarcinoma.