This is particularly evident in models of colitis-associated cancer, where Ackr2-deficient mice exhibit more severe experimental colitis and an increased cancer incidence due to heightened inflammatory chemokine production and excessive leukocyte infiltration.28 In colon adenocarcinoma, reduced Ackr2 expression correlates with elevated levels of CCL22, a chemokine that recruits regulatory T cells (Tregs), promoting an immunosuppressive tumor microenvironment. Here, CCL22 is linked to colitis.