In addition to alterations in the cytokine microenvironment, changes in cellular immune populations were also identified in the COPD samples, dysregulation of several genes in inflammatory pathways (AREG, IL6ST, S100A8/A9, SOCS1), and high levels of cytotoxic and exhaustion-related genes in CD4 and CD8 T Cells from COPD lungs. This evidence concerns the gene SOCS1 and chronic obstructive pulmonary disease.