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Obesity is defined as a BMI greater than 25 kg/m 2. Once thought to simply be a nutritional disorder, obesity has become a major health concern characterized by a state of constant low-grade inflammation caused by chronic adiposity. This state of inflammation is characterized by circulating inflammatory mediators, such as IL-6, leptin, and TNF-α, as well as varying levels of glucose-regulating hormones produced by obese adipose tissue. When left untreated, obesity can lead to a number of diseases including, but not limited to, cardiovascular disease, metabolic syndrome, neurodegeneration, type II diabetes mellitus, chronic kidney disease, and infertility. The distribution of adiposity differs in men and women, and these differences, along with the differences in sex hormones and sex hormone levels, can exacerbate or attenuate the course of disease pathology. Obesity can also be exacerbated by stress, which can worsen disease pathogenesis. In this review, we will explore how obesity affects inflammation and disease and how sex can affect the course of these diseases.

Cancer‐testis antigens (CTAs) are a group of genes that are normally expressed in the testis but aberrantly expressed in many different types of cancers. X‐linked antigens (XAGEs) are CTAs that are located on the X chromosome and that remain understudied and their role in cancer remains unclear. The specific expression of XAGEs in cancer cells make them a potential target for cancer therapy. The goal of this research project is to elucidate the biochemical function of XAGE genes and their protein products in normal and diseased states. We will first generate an atlas of cancer cell lines that display XAGE expression. Then we will perform gain and loss of function studies to determine what pathways are perturbed in the presence and absence of XAGEs. We will also determine binding partners of these proteins by IP‐Mass Spectrometry. In summary, our studies will shed light on the biochemical functions of the enigmatic XAGE proteins. Support or Funding Information HRD1764201

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