Likewise, the downregulation of PD-1 on CD4 + T cells and downregulation of PD-L1 in myeloid dendritic cells in patients with atrial fibrillation compared to healthy controls suggests that the downregulation of these checkpoints promotes T cell function and may contribute to the development or continuation of arrhythmias such as atrial fibrillation thru the mechanism of increasing cytokines such as IL-2 and IFN gamma, while suppressing regulatory cytokines such as IL-10 [38], potentially explaining how ICI-related arrhythmia events may transpire. The gene discussed is IL2; the disease is atrial fibrillation.