ENTPD1 and neoplasm: Infiltration of either n-Treg or i-Treg cells at inflammatory sites could potentially convert the 5′ AMP generated by CD39 expressed on neutrophils or dying cells into the anti-inflammatory mediator adenosine and, thus, dampening excessive immune reactions.[17–21] In any event for the expansion of tumor antigen-specific CTL response, blocking of the infiltration of Tregs at the tumor site is important.