Tsai et al. [28] noted that underhypoxic conditions, HIF-1α promotes AF by inducing phosphorylation ofc-Jun N-terminal kinase (JNK) and activator of transcription factor 2 (ATF2),along with the concomitant upregulation of proteins associated with fibrosis.Chen et al. [29] demonstrated that HIF-1α can enhance miR-210expression, inhibiting regulatory T cell (Treg) function via the targeting ofFoxP3, contributing to AF. Here, ATF2 is linked to atrial fibrillation.