CaMK-D was shown to inhibit EMT via the transcription factor Snail, as well as cytoskeleton remodeling, and to promote the migration and invasiveness of a variety of tumor cells, while different CaMK-D isoforms may exert opposite or identical effects on the progression of different kind of tumors, such as prostate, breast, skin, pancreatic, and gastric carcinomas (reviewed in [196]). This evidence concerns the gene CAMK2D and gastric carcinoma.