In GAPDH transgenic mice and in HCC murine models induced by DEN, GAPDH overexpression accelerated tumor development and progression by regulating inflammatory cytokines (Il-6, Il-1β, Mcp1, Icam1, Vcam1) at the transcriptional level and redirecting metabolic intermediates of glycolytic flux towards the one-carbon cycle, which is essential for cell proliferation [146]. Here, CCL2 is linked to neoplasm.