In contrast, IL-12/IL-23p40 subunit inhibition failed to show clinical benefit in multiple sclerosis, and IL-12/IL-23p40 or IL-23p19 subunit-targeted therapy failed to improve clinical outcomes in studies of patients with active rheumatoid arthritis, despite strong scientific rationale for this approach derived from animal models (31, 45, 108, 110). Here, IL23A is linked to multiple sclerosis.