Several mechanisms have been proposed to explain the reduction in corticosteroid response identified in patients with COPD, including upregulation of pro-inflammatory cytokines as a result of increased lung inflammation, reduced activity of corticosteroid receptor (GR), reduced expression of histone deacetylase-2, altered expression of surfactant protein D, and loss of Mucin 1 cytoplasmic tail expression [26,27,28]. This evidence concerns the gene SFTPD and chronic obstructive pulmonary disease.