Canakinumab preferably modulates NF-κB, IL-8 (CXCL8), MyD88, S100A9, and ATG5 predicted activity; these proteins are involved in processes of general innate immune inflammation, neutrophil recruitment and activation, and autophagy, all of them processes involved in Still’s disease pathophysiology [9, 11, 37], These signaling is predicted to involve both canonical and non-canonical IL-1 downstream molecular pathways. The gene discussed is ATG5; the disease is systemic-onset juvenile idiopathic arthritis.