Matrix-metalloprotease-cleaved Col1 (cCol1) and intact Col1 (iCol) play opposite roles in PC progression: cCol1 activates the discoidin domain receptor (DDR)1-NF-κB-p62-NRF2 signaling pathway, while iCol1 degrades DDR and disrupts this pathway [25]. This evidence concerns the gene DDR1 and pachyonychia congenita.