IL6 and atrial fibrillation: In vitro experiments showed that direct exposure of IL-6 to HL-1 cells induced the rapid decrease of the expression of Cx40 and Cx43, and that the expression of them rapidly recovered upon cessation of IL-6 exposure (Lazzerini et al., 2019), suggesting that IL-6 regulates the expression of gap junction channels on cardiomyocytes, and contributes to forming the AF substrate.