In vitro, siRNA-mediated knockdown of BCL6, DUSP3, and IL6R in Ang II-stimulated cardiac fibroblasts significantly suppressed their expression and attenuated fibroblast activation, while CUL4A knockdown showed supporting effects showing the pathogenic relevance of the core immune-regulatory axis in AF-ATH. The gene discussed is CUL4A; the disease is atrial fibrillation.