Related studies have shown that the key reasons for the individualized diversity of CS in humans are single nucleotide polymorphisms (SNPs) of nuclear receptor subfamily 3 group C member 1 (NR3C1), corticotropin-releasing hormone receptor 1 (CRHR1), glucocorticoid-induced transcript 1 gene (GLCC1), stress-induced phosphoprotein 1 (STIP1), histone deacetylase (HDAC), ATP-binding cassette transporter (ABC), and plasminogen activator inhibitor-1 (PAI-1). This evidence concerns the gene STIP1 and Cowden syndrome 1.