Over the past few years, several studies have described the expression of chemokine receptors in the skin and blood of CTCL patients, including the uniformly high expression of CC chemokine receptor 4 (CCR4) [7, 8, 9, 10] . CCR4 is highly expressed in both leukemic CTCL including Sézary syndrome and in MF, both in the very early stages (patch and plaque stages) of the disease and in large cell transformations [7, 8, 10, 11, 12] . It is also expressed on circa 60% of PC-ATCL cells [1] . In a recently published consensus article regarding the classification of CTCL, it is clear that CCR4 is expressed in the vast majority of CTCL cells, regardless of their histological subtype [1] . On the other hand, expression of CCR4 is limited amongst non-malignant cells [13] . It is not present on neutrophils, monocytes, or B cells [14] . It is absent on naïve T cells, and present on fewer than half of all memory T cells [15] . expression of CCR4 by tumor cells is associated with their skin involvement, CCR4 also has an important role in normal and tumor immunity [13, 14] . CCR4 is expressed at high levels on T regulatory cells (Tregs) that can migrate to tumor cells that secrete the CCR4 chemokines CCL17 and CCL21 to facilitate evasion from immune surveillance [16, 17] . High expression of the these CCR4 ligands has been detected in CTCL lesions [11] , breast cancer [16] , ovarian cancer [17] and oral squamous cell carcinoma [18] . Thus, targeted therapy against CCR4 may be an attractive treatment option for these malignancies, not only to directly kill the CCR4 + tumor cells, but also to overcome the suppressive effect of CCR4 + Tregs on the host antitumor immune response.