It was reported that the low CCL3L1 copy number is an important risk factor for HIV infection, whereas high CNV of CCL3L1 is protective against the disease.[22] A more recent publication reported the lower copy number (less than 2) of CCL3L1 increased the risk of SLE.[7] And another study suggested that CCL3L1 CNV was associated with the susceptibility to RA and T1D, probably through enhancing inflammatory responses and increasing the chance of autoimmune diseases.[6] Our present study showed there was indeed CCL3L1 CNV in GD patients and controls, from 1 copy to 5 copies. This evidence concerns the gene CCL3L3 and systemic lupus erythematosus.