This increase might result in an over‐activation of the C3a‐C3aR1 signaling in the endothelium, thus promoting vascular inflammation, increased BBB leakiness, lymphocyte infiltration,[274] and neurodegeneration.[275] Furthermore, in addition to their role in atherosclerosis progression, AT1 Agonistic Autoantibodies were revealed to contribute to the progression of vascular aging by stimulating the induction of senescence in ECs through the activation of AT1 receptors.[276]. The gene discussed is AGTR1; the disease is atherosclerosis.