Integrating these observations into this study on complement function in Fabry disease provides a broader context for understanding the specific roles of complement components, specifically the C3a and C5a mediated induction of ICAM1, VCAM1, and PECAM1, that could directly cause excess tissue recruitment of various immune cells, (e.g., macrophages, T cells, and B cells), driving inflammatory processes and promoting tissue damage in Fabry disease. Here, PECAM1 is linked to Fabry disease.