A transient metabolic switch induced the sustained expression of CA12 on macrophages via HIF1α- and autocrine cytokine-dependent pathways, and upregulated CA12 not only mediated the survival of macrophages in lactic acid–induced acidic culture conditions, but also directly facilitated HCC tumor metastasis and progression by inducing macrophage production of C-C motif chemokine ligand 8 (CCL8). This evidence concerns the gene HIF1A and neoplasm.