Celiac disease is a chronic inflammatory disease induced by ingested gluten from wheat, and similar proteins from barley and rye. An inappropriate immune response to gluten peptides leads to lymphocyte infiltration, villous atrophy and crypt hyperplasia in the small intestine. This gives symptoms as diarrhea, stomach pain and signs of malabsorption. The only, but very effective, treatment is gluten-free diet. The etiology is complex and not fully understood, but CD4+ T-helper cells and their recognition of gluten peptides on HLA-molecules is thought to play an important role. The only known genetic risk factor up until recently has been the HLA genes. There has been an intense hunt for more genes predisposing to celiac disease. But neither linkage studies nor traditional association studies have given clear answers. The introduction of genome-wide association studies (GWAS) have however started a new era in the investigation of complex diseases’ genetics, including celiac disease. Genome-wide association studies on celiac disease have so far found 11 new gene regions to have significant association with celiac disease. Almost all the new regions harbor genes with immunological functions. The strongest association has been shown for a region harboring IL2 and IL21, which both are good candidate genes. There has also been found that some genes are shared between immunological diseases, implying that there are common risk variants for these diseases. Further investigation with new genome-wide association studies and fine mapping and deep resequencing of the new gene regions will hopefully clear up the somewhat blurry picture we have of the etiology of celiac disease today. And with better understanding of the disease, often comes better diagnostic tools and treatment. One thing is for sure; scientists investigating celiac disease and other chronic inflammatory diseases have some interesting years ahead!