In addition to these recent advances in neurodegenerative research linking POP to AD and PD, this enzyme's proteolytic activity was also recently found to contribute to the release of acetyl-SDKP, a potent tetrapeptide that stimulates angiogenesis. It has since been reported that POP inhibition blocks the growth of human gastric cancer cells and the proliferation of breast cancer cells. We have also demonstrated that our own inhibitors (series based on 2 and 3, Figure ) can block POP protease activity in various cancer cell lines. The endopeptidase activity of POP is shared with FAP, the latter of which is suggested to be a key modulator of the tumor microenvironment (TME) and is thus a promising target for novel anticancer therapeutics. Discovered over 10 years after POP, FAP is overexpressed in most human epithelial-derived cancers and has also been suggested to promote tumor growth. In fact, its inhibition significantly affects stromal growth in vivo. Most importantly, FAP is not detectable in normal tissues, making it an extremely valuable target for therapeutic intervention against refractory tumors, and inhibitor development has in fact already started (Figure ).