Also, the over-expressed HRCR (heart-related circRNA) attenuates the development of cardiac hypertrophy and heart failure in mice by directly binding to miR-223 and acting as an endogenous super sponge to inhibit miR-223 activity, which results in the increasing expression of ARC, a target for miR-223, in heart cells [6]. The gene discussed is ARC; the disease is heart failure.