C7 is a critical component of the membrane attack complex (MAC), a multiprotein complex activated by the complement cascade that inserts into target cell membranes and forms pores leading to cell lysis 1. C7 serves as a membrane anchor during MAC assembly, associating with C5b and C6 to form the C5b-7 complex, a lipophilic precursor that interacts with the outer leaflet of target membranes and reduces energy required for membrane bending 2. The MAC is initiated by proteolytic cleavage of C5 into C5b in response to multiple complement pathways (classical, alternative, lectin, and GZMK), ultimately leading to phagocytosis and breakdown of pathogens while signaling to strengthen adaptive immunity 1. C7 expression is hepatically produced and regulated by C/EBPα transcription factor binding to specific promoter elements 3. Genetic deficiency of C7 impairs complement-mediated immune responses. Clinical significance is demonstrated in recessive dystrophic epidermolysis bullosa (RDEB), a genetic disorder caused by COL7A1 mutations affecting collagen VII, where gene therapy restoring C7 expression promoted wound healing and anchoring fibril assembly 4. C7 polymorphisms, particularly C7*3 (hypomorphic) common in Asian populations, may influence disease susceptibility to immunological and infectious disorders 5.