Our laboratory and others have shown that KO of FKBP52 in mice results in several pathological conditions, such as altered signaling of androgen receptor leading to hypospadias and reduced male fertility (Cheung-Flynn et al. 2005; Yong et al. 2007), reduced progesterone receptor activity leading to defective uterine implantation (Tranguch et al. 2005; Yang et al. 2006), and reduced GR activity leading to increased susceptibility to diet-induced steatosis (Warrier et al. 2010). The gene discussed is FKBP4; the disease is steatosis.