For instance, conditions such as nonalcoholic fatty liver disease and metabolic syndrome further suggest that inflammation is a significant predictor of the microenvironment in which AF is sustained.[13] In the context of inflammatory regulation in AF, low expression of PD-1 on predominantly CD4+ T cells has been observed to promote T-lymphocyte activation and increase the inflammatory load in vivo. The gene discussed is CD4; the disease is atrial fibrillation.