In FLS, Ca2+-activated potassium channels appear to drive invasiveness of synoviocytes and progression of arthritis in both human and rodent RA models (Petho et al., 2016; Tanner et al., 2019), by increasing production of both inflammatory mediators and catabolic enzymes (Hu et al., 2012; Friebel et al., 2014; Tanner et al., 2015). This evidence concerns the gene KCNA3 and rheumatoid arthritis.