In the possible survival of epithelial cells in the androgen-poor environment. Maldonado and collaborators have characterized the capacity of prostate stromal cells to recognize and respond to pathogenassociated molecular patterns, given the characteristic pattern of Toll-like receptor 4 expression. They also extended the observations to determine the effects of castration, and showed that RELA, in combination with CD14 and MyD88, coordinates the adaptation of epithelial and smooth-muscle cells to androgen deprivation, including the ability to produce surfactant protein D. The results reported here are in good agreement with these functional assays. They add an extra layer to the mechanisms regulating the ability of the prostate to deal with infectious agents, and reinforce the notion that the epithelium and stroma perform complementary and perhaps overlapping functions as an immune barrier. It will be interesting to determine how these functions correlate with the gland function to produce and secrete antiinflammatory factors, as well as their variations and function in human prostatitis. Nonetheless, we suggest that the combined functions of these TF regulate the recruitment of immune cells to the organ and also the functioning of these immune cells, including the ability to concentrate immunoglobulins in the secretion. NFYB forms ternary complexes with NFYA and NFYC. NFYB shows interaction with p53, with significant overlapping target genes in HCT116 cells, with emphasis on ER-stress regulators and regulators of p53 itself. Notably, NFYB interacts with p53 to downregulate Chk2, which is associated with DNA damageinduced cell cycle progression in G2, and specifically targets cdc25 and p53, and p73 to block the PDGFB receptor. It will be interesting to investigate how NFY is involved in the reported dissociation of p53 and apoptosis in prostate regression after castration. Taken together, the present data reveal novel TF that may contribute not only to prostate carcinogenesis and progression to CRPC, but also to the regulation of gene expression during the physiological adjustment of this organ to androgen variations in seasonal reproducers or in social groups with a male hierarchy. Type 2 diabetes is one of the most common chronic diseases worldwide and is associated with an increased risk for cognitive decline and dementia. Chronic hyperglycemia and alterations of cellular homeostasis, characteristic of T2D, lead to diffuse vascular damage and multi-organ dysfunction. Hyperglycemia is a key determinant of both macrovascular and microvascular complications of T2D, and there is extensive evidence showing that both acute and chronic hyperglycemia are deleterious. Hemoglobin A1c levels, even in non-diabetic individuals, are associated with cognitive performance and brain volume. Based on the beneficial effect of good glycemic control in preventing other diabetes complications.