Juvenile idiopathic arthritis (JAL4) is the most common chronic rheumatologic disease in children. JIA is a group of disorders that share the clinical manifestation of chronic joint inflammation. The Human Leukocyte Antigen region (HLA) seems to be a major susceptibility locus for JIA that is estimated to account for 17% of familial segregation of the disease. Genome-wide association studies (GWAS), case-control studies and meta-analyses of the post-GWAS era revealed over 20 non-HLA loci conferring susceptibility to JIA. At least a half of those are shared between JIA and rheumatoid arthritis, an adult rheumatic disease, thereby suggesting for similarity of pathogenic mechanisms of both diseases. New findings also suggest for a likely role of epigenetic alterations in the pathogenesis of JIA that should be investigated in the future.