TGFB1 and Dystrophic epidermolysis bullosa: The findings of another study implicate the disruption of several interconnected biological processes due to the absence of type VII collagen, including chronic inflammation stemming from impaired wound healing, dysregulation of TGF-β signaling cascades, and abnormalities in immune function, all of which could contribute to the development of cSCC in dystrophic epidermolysis bullosa (DEB) patients [111].