Yoshioka et al. traced deletion of ITGB4 back to defective signaling of ErB2 and c-Met in prostate tumor progenitor cells; inhibition of ErbB2 and c-Met subsequently reduced the ability of tumor progenitor cells to self-renew in vitro, suggesting ITGB4 signaling may play a critical role in maintaining CSC within the tumor [23, 24]. This evidence concerns the gene ITGB4 and neoplasm.