Kawasaki　disease　(KD)　or　Kawasaki　syndrome　is　known　as　a　vasculitis　of　small　to　medium-sized　vessels,　and　coronary　arteries　are　predominantly　involved　in　childhood.　Generally,　20-25%　of　untreated　with　IVIG　and　3-5%　of　treated　KD　patients　have　been　developed　coronary　artery　lesions　(CALs),　such　as　dilatation　and　aneurysm.　Understanding　how　coronary　artery　aneurysms　(CAAs)　are　established　and　maintained　in　KD　patients　is　therefore　of　great　importance.　Upon　our　previous　genotyping　data　of　157　valid　KD　subjects,　a　genome-wide　association　study　(GWAS)　has　been　conducted　among　11　(7%)　CAA-developed　KD　patients　to　reveal　five　significant　genetic　variants　passed　pre-defined　thresholds　and　resulted　in　two　novel　susceptibility　protein-coding　genes,　which　are　NEBL　(rs16921209　(P　=　7.44　x　10(-9);　OR　=　32.22)　and　rs7922552　(P　=　8.43　x　10(-9);　OR　=　32.0))　and　TUBA3C　(rs17076896　(P　=　8.04　x　10(-9);　OR　=　21.03)).　Their　known　functions　have　been　reported　to　associate　with　cardiac　muscle　and　tubulin,　respectively.　As　a　result,　this　might　imply　their　putative　roles　of　establishing　CAAs　during　KD　progression.　Additionally,　various　model　analyses　have　been　utilized　to　determine　dominant　and　recessive　inheritance　patterns　of　identified　susceptibility　mutations.　Finally,　all　susceptibility　genes　hit　by　significant　genetic　variants　were　further　investigated　and　the　top　three　representative　gene-ontology　(GO)　clusters　were　regulation　of　cell　projection　organization,　neuron　recognition,　and　peptidyl-threonine　phosphorylation.　Our　results　help　to　depict　the　potential　routes　of　the　pathogenesis　of　CAAs　in　KD　patients　and　will　facilitate　researchers　to　improve　the　diagnosis　and　prognosis　of　KD　in　personalized　medicine.