Depression is one of the most common diseases worldwide with over 300 million people currently diagnosed. Currently, all depression is being treated the same even though depression can manifest itself in several different combinations. To be diagnosed with depression, a patient needs to have just 5 of the 9 symptoms defined by the American Psychiatric Association DSM-5. This means there are 256 possible combinations of depressive symptoms that could be presented by an individual. One observation that has been made is that individuals with diseases that cause too much or too little of the stress hormone cortisol often show signs of depression; this led us to our hypothesis that genetic factors related to cortisol levels, function, or activity may increase someone's risk for depression. In order to find better treatments for depression it is first necessary to have a better understanding of the different types of depression and the role of genetics in the hypothalamic-pituitary-adrenocortical axis (HPA-axis) that regulates cortisol levels and the different mechanisms by which cortisol action is regulated. Hypersensitivity is experienced when an individual's body reacts to a normal amount of cortisol as if it were an abundance of cortisol while resistance refers to someone who does not respond fully to normal amounts of cortisol. We can determine hypersensitivity and resistance by looking at single nucleotide polymorphisms (SNPs)- changes in the sequence of the DNA in some genes; our lab is interested in the contribution to depression of SNPs in several genes including the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR). If a patient expresses GR resistance and MR sensitivity (or vice versa) the contrasting effects could result in dysregulation of the stress response. By better understanding how dysregulation of the HPA-axis contributes to depression, we can begin to answer our research question: how do we better treat depression.