GAL2R strongly exerted anti-tumor activity via two important mechanisms: (1) tumor cell cycle arrest mediated via the extracellular-regulated protein kinase-1/2 (ERK1/2)-dependent effects on the cyclin-dependent kinase inhibitors (CKI) and cyclin D1, and (2) induction of caspase-3-dependent apoptosis [20]. Here, CHKA is linked to neoplasm.