In conclusion, regarding all cellular event outcomes, a possible mechanism of action of CrataBL involves its capacity to bind to highly expressed matrix components at the tumor site, decreasing the adhesion of melanoma cells to laminin, directly or indirectly inhibiting the activity of various proteases (such as cathepsins and kallikrein 7) in the tumor cells, and blocking some key signaling proteins that decrease the proliferation, migration, invasion, and survival of SK-MEL-28 cells. This evidence concerns the gene LAMB2 and neoplasm.