Since in our previous study we found that PEDF, a lipolysis-mediating protein known to suppress tumor progression, was able to normalize the MTOC number in both PCa cells and prostate stromal cells by reducing pericentrin and centrin 1 proteins to a single focus per cell, we tested potential signaling mechanisms responsible for the ability of PEDF to alter MTOCs. The gene discussed is CETN1; the disease is posterior cortical atrophy.