TGFB1 and recessive dystrophic epidermolysis bullosa: This was compatible with the inflammatory state, the upregulation of TGFβ, and the tissue remodeling in the absence of C7 expression that has been reported in RDEB patient keratinocytes and fibroblasts12,36, and indicated that RDEB_L1 cells were recapitulating the main expected disease signatures of RDEB.