Additionally, the overexpressed COL4A1 or COL4A2 could activate pathways in cancer including notch, platelet activation, cGMP-PKG, PI3K-Akt, focal adhesion, actin cytoskeleton, and ECM-receptor interaction (Figure 9C), which was consistent with the above biological pathways activated by COL4A1 and COL4A2 (Figure 7D). This evidence concerns the gene COL4A2 and cancer.