D6/ACKR2 overexpression in ATC cells causes a dramatic loss of their ability to recruit leukocytes in vitro and in vivo, indicating that the miR-146a-mediated inhibition of D6/ACKR2 expression ensures the retention of elevated chemokine levels in tumor microenvironments to promote high rate leukocyte recruitment for thyroid cancer progression [68]. Here, ACKR2 is linked to thyroid cancer.