For instance, in cystic fibrosis, the CFTR Phe508del mutation induces the in-frame deletion of phenylalanine 508, resulting in endoplasmic reticulum retention and the proteasomal degradation of misfolded CFTR protein, ultimately causing exocrine gland mucus viscosity through impaired membrane trafficking [32]. The gene discussed is CFTR; the disease is cystic fibrosis.