C4A is a complement component generated through proteolytic cleavage during classical complement pathway activation 1. While structurally similar to anaphylatoxins C3a and C5a, C4A has a distinct functional profile 2. Unlike C4B, which preferentially binds carbohydrate antigens through ester bonds, C4A preferentially binds to immune complexes and protein antigens through amide bonds 34, facilitating immune complex solubilization and clearance via complement receptor 1 on erythrocytes 4. Recent evidence reveals an unexpected role: C4a binds oxytocin and modulates plasma oxytocin concentrations, affecting social behavior in mice 5. In the brain, C4A participates in synaptic refinement and pruning 6. C4A overexpression promotes excessive synaptic elimination through microglial engulfment, potentially contributing to abnormal brain circuit development and behavioral changes 6. Increased C4A brain expression is associated with schizophrenia risk 6, and functional variants affecting C4A regulation have been implicated in Alzheimer's disease pathogenesis 7. Clinically, C4A deficiency is a strong genetic risk factor for systemic lupus erythematosus (SLE), with homozygous C4A null alleles more frequent in SLE patients, likely due to defective immune complex processing 83. Additionally, increased C4A gene copy number correlates with elevated C4 protein expression in Alzheimer's disease patients 9.