The novelty of the current study lies in the fact that we tried to modulate the genes KLK2, KLK4, KLK6, and KLK14 to inhibit the progression of PCa via miR-378, which can be produced in tumor cells through EPA, stimulating co-expression of the gene PGC-1β [2]. The gene discussed is KLK2; the disease is posterior cortical atrophy.