Eradication of a disease (e.g., rabies) brings the greatest health benefit, which is the absence of the health threat. It is also the quintessential example of health equity, as all mankind reaps the benefits, leading to eternal cost savings. Rabies is undoubtedly the most feared zoonosis in the world, and takes a heavy toll on underprivileged communities living in the poorest countries. The expertise to reduce the global burden of rabies has been built, and significant strides have been made scientifically and practically towards eliminating canine rabies and reducing human rabies deaths in the industrialized world. Moreover, considerable milestones have been achieved towards taking this progress to the next level, by reducing the dramatic impact of rabies on human and animal communities in endemic areas of the developing world. In an effort to enact a "One Health" approach towards global rabies elimination, the creation of effective partnerships has focused on coordinating research and operational activities related to canine rabies elimination. A global rabies network, covering over 150 countries, and uniting stakeholders from the spectrum of veterinary, public health, pharmaceutical, animal welfare, and wildlife conservation agencies, as well as local communities, has been established. Strategies and tools to successfully prevent and control rabies have been formulated to assist rabies-affected areas in management efforts. Operational activities have been implemented in a diversity of Asian, African, and Latin American settings to create replicable and sustainable models, acting as exemplary showcases for others. More broadly, current strategies towards rabies elimination have the potential to be used as a modern example of integrated, evidence-driven, research-based approaches applicable to other major zoonotic pathogens affecting global health. While access to tools and knowledge has been increased, providing all countries with the potential to eliminate rabies from their territories, the ultimate achievement of this goal, which would lead to health equity, continues to face many challenges. Political and financial constraints remain, highlighting the need for further action towards building the political will to eliminate rabies and to create sustainable and economic solutions, to develop additional practical research tools, and to attract long-term national and international funding support. Interplay between SIN3A and STAT3 Mediates Chromatin Conformational Changes and GFAP Expression during Cellular Differentiation BACKGROUND: Neurons and astrocytes are generated from common neural precursors, yet neurogenesis precedes astrocyte formation during embryogenesis. The mechanisms of neural development underlying suppression and de-suppression of differentiation- related genes for cell fate specifications are not well understood. METHODOLOGY/PRINCIPAL FINDINGS: By using an in vitro system in which NTera-2 cells were induced to differentiate into an astrocyte-like lineage, we revealed a novel role for Sin3A in maintaining the suppression of GFAP in NTera-2 cells. Sin3A coupled with MeCP2 bound to the GFAP promoter and their occupancies were correlated with repression of GFAP transcription. The repression by Sin3A and MeCP2 may be an essential mechanism underlying the inhibition of cell differentiation. Upon commitment toward an astrocyte-like lineage, Sin3A- MeCP2 departed from the promoter and activated STAT3 simultaneously bound to the promoter and exon 1 of GFAP; meanwhile, olig2 was exported from nuclei to the cytoplasm. This suggested that a three-dimensional or higher-order structure was provoked by STAT3 binding between the promoter and proximal coding regions. STAT3 then recruited CBP/p300 to exon 1 and targeted the promoter for histone H3K9 and H3K14 acetylation. The CBP/p300-mediated histone modification further facilitates chromatin remodeling, thereby enhancing H3K4 trimethylation and recruitment of RNA polymerase II to activate GFAP gene transcription. CONCLUSIONS/SIGNIFICANCE: These results provide evidence that exchange of repressor and activator complexes and epigenetic modifications are critical strategies for cellular differentiation and lineage-specific gene expression. During embryonic development, the generation of three major neural cell types (neurons, astrocytes, and oligodendrocytes) in the central nervous system (CNS) sequentially occurs, whereby almost all neurons are generated before the appearance of glial cells [1, 2] . Recent findings demonstrated that glial cells are important in critical neuronal maturation processes such as axonal pathfinding, synapse formation, neurotransmitter transport, metabolic functions, and the response to CNS injury [3] [4] [5] [6] . Although rodent brain cultures and neuronal and glial cell lines have provided us with important information about the structure and function of the mammalian CNS, we have scanty understanding of astrocytic differentiation.