Capitalizing on the critical contribution of the CCL17-CCR4 chemokine axis in ATLL, the use of CCL17 fused to an exotoxin of Pseudomonas was shown to kill HTLV-1-infected cells in a CCR4 and furin-dependent manner [157], and the design of T cells expressing a chimeric antigen receptor that targets CCR4 demonstrated its efficiency in lysing autologous patient-derived tumor cells [158]. This evidence concerns the gene CCR4 and neoplasm.