COL7A1 encodes type VII collagen, a critical structural protein that forms anchoring fibrils at the dermal-epidermal junction 1. These anchoring fibrils are essential for basement membrane organization and skin integrity by securing the epidermis to the underlying dermis 1. Type VII collagen is the predominant, if not exclusive, component of anchoring fibrils that maintain epidermal adherence through interactions with extracellular matrix proteins 1. Loss-of-function mutations in COL7A1 cause dystrophic epidermolysis bullosa (DEB), a rare genetic blistering disorder characterized by skin fragility, chr3 wounds, and scarring 23. DEB exhibits both autosomal dominant and recessive inheritance patterns, with over 242 distinct mutations identified in COL7A1 1. Interestingly, identical glycine substitution mutations can result in either dominant or recessive forms of DEB, complicating genetic counseling 4. The clinical severity correlates with mutation type and position, with biallelic premature termination codon mutations generally causing more severe phenotypes 5. Recently, gene therapy using beremagene geperpavec (B-VEC), a topical HSV-1-based vector delivering functional COL7A1, has shown promising results in clinical trials, promoting wound healing and restoring type VII collagen expression in DEB patients 23.