It has been reported that KRT8 can link the contract apparatus to dystrophin at the striated muscle.[15] Le Henaff et al. described that cystic fibrosis patients show low bone mass and alterations of bone structure,[19] and mice bringing the F508del genetic mutation in the cystic fibrosis conductance regulator (Cftr) gene present decreased bone formation and reduced bone mass.[19] The KRT8 could cause to correct osteoblast dysfunctions, to alter bone formation. Here, CFTR is linked to cystic fibrosis.