Previous studies have identified effector cell states in rheumatoid arthritis pathophysiology that represent promising treatment targets, including HBEGF+IL1B+ macrophages, SLAMF7+ super-activated macrophages, MERTK+ macrophages, CD11c+ autoimmune-associated B cells (ABCs), PD-1hi T peripheral helper (TPH) cells, granzyme K+CD8+ T cells and NOTCH3+ synovial fibroblasts8–16. This evidence concerns the gene CD8A and rheumatoid arthritis.