The C-type lectin-like super domain (CTLD) family has diverse functions, and in particular, is important in innate immunity including nature killer (NK) function or pathogen recognition [25] . CLEC5A belongs to the Group V "NK cell receptors" family, and MDL-1 expression is upregulated in activated myeloid cells [26] and acts as a signaling receptor for proinflammatory cytokine and chemokine release [14] . Even though a number of reports have demonstrated that KD involves activation of a wide array of immunological elements such as T cells and macrophages [16] [17] [18] 27] , with the subsequent release of several cytokines [28] , only a few reports have addressed the role of lectin in the pathogenesis of KD. Several genetic associations with susceptibility to KD and CAL formation have been reported, but the results are inconsistent [29] [30] [31] [32] . Previous genetic association studies have indicated that the intronic SNP (rs28493229) of ITPKC, 1,4,5-trisphosphate 3-kinase C, reduces gene expression by altering splicing efficiency, and the C allele contributes to immune hyperreactivity in KD patients [29] . Recently, it has been demonstrated that rs28493229 is associated with susceptibility to KD and CAL formation [24, 29] . ITPKC is able to regulate the immune system via calcium-dependent NFAT pathways [29] . Similarly, previous studies have indicated that C-type lectin receptors (CLRs) are critical in the activation of the Syk-mediated NFAT signaling pathway [33] . In addition, CLEC5A has been shown to play a key role in host defense and to be involved in dengue virusmediated disease [14] . This finding suggests CLEC5A may be a potential target protein that involves calcium-dependent immune regulation and contributes to the development of coronary artery lesions. However, we did not find evidence to support a genetic role of CLEC5A in the pathogenesis of KD. Since we picked tagging SNPs from the HapMap database, only the tagging SNPs with a minor allele frequency of more than 10% were selected. Although our tSNP could capture majority of the underlying genetic variances with MAF > 10% across the CLEC5A gene, the rare causal genetic polymorphisms in CLEC5A may not have been detected in this study. Therefore, we cannot rule out or exclude rare causal genetic polymorphisms in CLEC5A. In addition, there are, at least, seventeen groups of CLRs in vertebrates. Indeed, it has been reported that mannose-binding lectin gene polymorphisms are associated with susceptibility to KD [34] and CAL formation [35] . Thus, large-scale DNA sequencing to CLR family is needed to better understand KD.