Mechanisms for galectin-3 overexpression in cancer cells remain unclear, although several transcription factors, such as Sp1, cAMP response element-binding protein, nuclear factor (NF)-κB, activator protein (AP)-1, Runx2, and Ras/mitogen-activated protein kinase (MAPK) signaling, have been suggested to be involved [8], while p53 shows negative regulation of galectin-3 [41, 42]. This evidence concerns the gene LGALS3 and cancer.