In prostate cancer cells, colorectal cancer cells, and osteosarcoma cells, the methyl donor AdoMet is able to reverse the hypomethylated state of prometastatic genes, including urokinase-type plasminogen activator (uPA) and zinc-dependent matrix metalloproteinases (MMPs), which play a key role in the degradation and remodeling of the extracellular matrix and are also involved in the modulation of all stages of carcinogenesis, from tumor initiation to metastasis [26,27,28]. This evidence concerns the gene PLAU and prostate carcinoma.