NFKB1 and atrial fibrillation: The existence of such a mechanobiological threshold is further supported by Wang et al., who reported that moderate cyclic tensile stretch (5%) of AF cells stimulates YAP and represses the NF-κB pathway, which leads to a decrease in inflammatory levels and an increase in ECM synthesis and cell proliferation [21], whereas overloading (12%) leads to YAP inactivation, increased NF-κB signaling, inflammation and catabolic responses.