However, it is also known that genetic variability in inflammatory genes, such as IL-6, IL-11, and TNF-α, as well as in enzymes involved in the prostaglandins and kynurenine pathways, contributes to both the risk of depression and to antidepressant response (Bull et al., 2009; Dowlati et al., 2010; Uher et al., 2010; Bufalino et al., 2013), thus suggesting that a different cluster of individuals expresses high levels of inflammation and lack of treatment response through a predominantly genetic path. Here, IL11 is linked to depressive symptom measurement.