In addition, the intracellular trafficking of cathepsin B appeared frequently altered in malignant tumors [32], resulting in i) an increased secretion of precursor and active forms of the enzyme [33], ii) its redistribution from perinuclear lysosomes to peripheral vesicles localized in invadopodes [34], and finally iii) its association with the plasma membrane [35], where it was found associated to the caveolae, via active K-RAS, at least in colon cancer [36]. The gene discussed is KRAS; the disease is malignant colon neoplasm.