For example, supraspinatus tendon samples from patients with early-stage tendon disorders displayed a mixed inflammation signature with increased expression of genes and proteins mediated by interferon and the NF-κB signaling pathway; intermediate-stage tendon disorders showed an inflammation signature where expression of the NF-κB mediated proinflammatory genes and proteins; advanced-stage tendon disorders showed the increased expression of STAT-6 and glucocorticoid receptor pathway (108). This evidence concerns the gene STAT6 and disease of the tendon.