Possible mechanisms for the discrepancy between systemic endocan and p14 endocan levels in acute leukemia patients could be altered or additional endocan degradation by other proteinases than cathepsin G [30,46], inhibition of cathepsin G activity by increased release of protease inhibitors (e.g., by the leukemic cells) [46], or altered cellular or extracellular matrix adhesion/binding of the p14 fragment. This evidence concerns the gene CTSG and acute leukemia.