Specifically, for compound 2, we can conclude that inhibition of Src signaling cascade, inhibition of hypoxia-inducible factor-1 alpha (HIF-1α) synthesis, and inhibition of androgen-dependent/independent mechanisms are the main modes of CS action for non-small-cell lung cancer, hepatoma Hep3B cells, and prostate cancer cells, respectively [147]. This evidence concerns the gene HIF1A and prostate cancer.