This AHR signal increases CCR2 and CD39, an ATP/ADP-degrading ectonucleotidase, expression on TAMs, resulting in increased CCL2-induced TAM recruitment into the tumor microenvironment and subsequent rise in the environmental adenosine concentration by the ectonucleotidase activity of CD39/CD73; all of which contributes to tumor progression by suppressing T-cell immunity [31]. The gene discussed is AHR; the disease is neoplasm.