In in vitro study, Lu et al. [9] showed enhanced apoptosis and inhibited GSK-3β phosphorylation to down-regulate both β-catenin and cyclin D1 with fat-1 gene transfer directly into prostate cancer cells and in in vivo study using a melanoma xenograft model, Xia et al. [6] showed that the anti-tumor action of ω-3 PUFAs was mediated through apoptosis via the activation of the Phosphatase and tensin homologue deleted on the chromosome 10 pathway. Here, CCND1 is linked to prostate cancer.