11,12-EET was found to induced prostate carcinoma cell spreading and the formation of actin-myosin microfilaments possibly by the trans-activation of EGFR and PI3K/AKT pathways, which could account for the observed effects on cell invasion and migration.399 Blocking EET synthesis or activation using EET antagonists such as 14,15-EEZE, on the other hand, caused the cells to become more rounded and smaller.399 Together, these data suggest that CYP inhibition may represent a novel approach to prevent metastasis of human cancers. This evidence concerns the gene AKT1 and cancer.