Our initial research on the role of Gal-3 in PBC pathogenesis has demonstrated that Gal-3 deletion exacerbates cholangitis in 2-octynoic acid coupled to BSA immunized C57BL/6 mice by enhancing apoptosis of cholangiocytes followed by enhanced autoantigen release and increased stimulation of antigen presenting cells (9). This evidence concerns the gene LGALS3 and primary biliary cholangitis.