However, given the marked patient-level heterogeneity, we developed methods called UDON and SATAY-UDON to identify and describe novel disease-associated transcriptional programs implicating what we believe to be new potential drivers of SJIA pathogenesis, including IFN activation, multiple distinct monocyte phenotypes, and platelet activation. The gene discussed is IFNA1; the disease is systemic-onset juvenile idiopathic arthritis.