Furthermore, our results demonstrate for the first time that relaxin-2 treatment inhibits normal human atrial cardiac fibroblasts migration (which is in concordance with previous findings in rat cardiac fibroblasts34) and, additionally, reduces TGF-β1 mRNA and protein expression in our cells, in agreement with the proposed role for relaxin-2 in the disruption of the pro-fibrotic TGF-β1/IL-1β axis35, underpinning a potential therapeutic use of relaxin-2 for the inhibition of cardiac fibrosis, which could be suitable for AF management. Here, RLN2 is linked to atrial fibrillation.