There has been some evidence demonstrating the role of DC-SIGN promoter variants in the susceptibility to or the protection against various infectious diseases, such as dengue fever, tuberculosis, and AIDS [7] [8] [9] . However, whether DC-SIGN promoter variants have effects on susceptibility to KD is still unknown. Since DC-SIGN, also known as CD209, is so important for the anti-inflammatory functions of IVIG, it is reasonable to hypothesize that a functional single nucleotide polymorphism (SNP) in the CD209 molecule will be involved in the pathogenesis of KD or response to IVIG treatment. We hypothesized that the SNP rs4804803 of DC-SIGN promoter may be involved in the susceptibility to KD, CAL formation, coronary artery fistula formation, and IVIG treatment response in KD patients. To test this hypothesis, we conducted a case-control study involving 278 patients with KD and 243 controls.