Research has consistently demonstrated elevated levels of complement components, including complement 1q subcomponent c (C1qc), C3, inactivated C3b (iC3b), C4, and complement factor B (CFB), alongside the production of complement fragments C3a and C5a, in serum, plasma, and tissue samples from both animal models and human patients with Fabry disease (Table 1). Here, CFB is linked to Fabry disease.