We were then able to ask whether any combination of endonexin-fold mutations (i) suppressed the ability of ANXA7 to fuse artificial membranes; (ii) inhibited proliferation of prostate cancer cells; (iii) sensitized prostate cancer cells to cell death; and (iv) identified signaling pathways that were responsible for the tumor suppressor function. This evidence concerns the gene ANXA7 and neoplasm.