Further underlining the importance of the CCL17/CCL22/CCR4 signaling axis in ATLL pathogenesis, somatic gain of function (GOF) mutations in CCR4, detected in 26 to 29% of ATLL cases [102,103], result in increased cell migration toward CCL17 and CCL22, together with impaired CCR4 internalization [102]. Here, CCL22 is linked to adult T-cell leukemia/lymphoma.