Starting with monocytes, extracellular acidosis suppresses the expression of monocyte chemoattractant protein-1 (MCP1) and IL-6, both of which are critical for the maintenance of the pro-inflammatory M1 macrophage phenotype in the TME while at the same time promoting M1 to tumor-associated macrophage (TAM/M2) subtype transformation by increasing mannose receptor C-type 1 and arginase 1 expression [31,32]. Here, MRC1 is linked to neoplasm.