These include the induction of apoptosis in different animal models, inhibition of the phosphorylation of c-Jun and ERK1/2 in lung tumorigenesis models, suppression of phospho-AKT and nuclear β-catenin levels in colon cancer models, inhibition of the IGF/IGF1R axis in colon and prostate cancer models, and suppression of VEGF-dependent angiogenesis in lung and prostate cancer models [19,22,24,29,121]. This evidence concerns the gene JUN and prostate carcinoma.