Indeed, although the production of MMP9 by peripheral blood mononuclear cells (PBMCs) was found constitutively augmented in CF patients homozygous for F508del mutation because of impairment in PBMCs Ca2+ homeostasis, NE potentiates MMP9 activity through a direct activatory cleavage and/or the degradatory cleavage of its inhibitor, the tissue inhibitor of metalloprotease-1 (TIMP-1) with subsequent augmented collagen degradation and tissue damage [71,93,94,95,96]. The gene discussed is MMP9; the disease is cystic fibrosis.