Increased Bad and AR phosphorylation by the activation of PI3K/Akt and ERK signaling pathways upon Vav3 stimulation contributes to prostate cancer growth under chronic hypoxia (Figure 6A), whereas increased Bcl-2 phosphorylation and decreased Bad phosphorylation through the activation of JNK signaling by docetaxel coupled with decreased phosphorylation of Bad and AR through the inhibition of PI3K/Akt and ERK signaling pathways upon the addition of si-Vav3 contributes to increased apoptosis (Figure 6B). This evidence concerns the gene VAV3 and prostate cancer.