Cleavage of collagen-like domain of Gal-3 by matrix metalloproteases (MMP), MMP-2 and MMP-9 (Ochieng et al., 1994; Nangia-Makker et al., 2008; Nangia-Makker et al., 2010) and prostate specific antigen (PSA) (Balan et al., 2012) enhances interactions of larger Gal-3 fragments with proteins leading to enhanced heterotypic aggregation, chemotaxis, and consequently tumor progression (Nangia-Makker et al., 2008; Nangia-Makker et al., 2010). The gene discussed is LGALS3; the disease is neoplasm.