TNF and recessive dystrophic epidermolysis bullosa: These include growth activation of keratinocytes, polymorphisms in matrix metalloproteinases, and compromised immune surveillance with reduced activity of natural killer cells.[57, 58, 59, 60, 61, 62 The chronic inflammatory state, with lead mediators in RDEB including transforming growth factor‐β (TGF‐ß), tumor necrosis factor α (TNF‐α) and IL‐6, is implicated in the biophysically altered, fibrotic tissue microarchitecture, which is characterized by matrix stiffening, aberrations of mechano‐signalling and enhanced epithelial‐to‐mesenchymal transition in keratinocytes.