The KAP gene is exclusively expressed in proximal tubules of mouse kidney and in the uterus of pregnant females before they give birth. It displays an exquisite and differential regulation of expression by steroid and thyroid hormones in different proximal tubule segments. While the pars recta (PR cells) responds to thyroid and sexual hormones, the pars convoluta (PCT cells) represents a truly androgen-dependent compartment, since expression occurs only in the presence of androgens and functional androgen receptors. Nevertheless, different hypothyroidism models have indicated that thyroid hormone (TH) might also contribute to the androgenic response in PCT cells. In the present study, we aimed to determine the molecular mechanisms that ultimately control KAP expression in these cells. Using several genetically-deficient mouse models and different pharmacologic and hormonal treatments, we determined that thyroid and growth hormone (GH) modulate c/EBP and levels which, in turn, control KAP expression in PCT cells in a developmentally-dependent manner. We demonstrated that these factors bind to sites in the proximal KAP promoter, thereby collaborating with androgens for full KAP expression. Finally, we propose that TH and GH, acting through c/EBPs, may constitute a general regulatory mechanism of androgen-dependent genes in mouse kidney.