A genetic predisposition is suggested based on clinical and epidemiologic features [1, 26] . In this study, we investigated whether the polymorphism of DC-SIGN (CD209) promoter −336 A/G (rs4804803) was associated with susceptibility and CAL formation in KD. Our study showed that the allele −336G was associated with susceptibility to KD. To the best of our knowledge, this is the first study to explore the association between DC-SIGN polymorphisms and susceptibility to KD. Immunoglobulin is well known for its defensive role in pyogenic infection. In addition to its protective role, immunoglobulin G (IgG) was also noted to have anti-inflammatory effects at high doses. Recently, the α2, 6 sialylated IgG was reported to interact with a lectin receptor, SIGN-R1 in mice and DC-SIGN in humans, and to trigger an antiinflammatory cascade. Thus it is reasonable to hypothesize that a functional SNP in the DC-SIGN molecule will be involved in the response to IVIG treatment. However, in our study, we found the variant and haplotype of −336A/G in the DC-SIGN gene did not associate with the occurrence of IVIG resistance or CAL formation in KD. Because of its highly polymorphic nature and numerous SNPs of DC-SIGN gene 4