Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease linked to type 2 diabetes (T2D), obesity, and dyslipidaemia, which are all parts of the metabolic syndrome. In 2024, for non-cirrhotic MASH with mild to advanced fibrosis, resmetirom, a selective thyroid hormone receptor-β agonist, became the first FDA-approved treatment for this condition. By increasing β-oxidation and lipid metabolism, it minimises systemic thyroid or cardiac effects while reducing hepatic fat, inflammation, and fibrosis. Resmetirom is being developed for use in combination with lifestyle interventions, such as diet and exercise, to maximize patient benefit. Nevertheless, the lack of congruence between clinical trial populations and real-world payer criteria underscores access obstacles that necessitate policy reform. The successful delivery of screening programs depends on the education of providers from various disciplines and the establishment of uniform screening standards. Future studies should investigate the clinical application of resmetirom in combination with agents that may provide additional benefits, such as GLP-1 receptor agonists, SGLT2 inhibitors, and statins. These results are significant in light of recent long-term safety monitoring of these agents, particularly regarding the thyroid axis. Ensuring equitable uptake will be crucial, as it involves defining fair access through payer endpoints, conducting cost-effectiveness analysis, and considering patient-reported outcomes. Resmetirom represents a breakthrough in MASH management, offering potential metabolic benefits in conjunction with comprehensive clinical and lifestyle approaches.

The gut microbiota plays a critical role in maintaining gastrointestinal homeostasis, immune regulation, and metabolic processes. Recent evidence has highlighted its significant influence on gastric carcinogenesis. Helicobacter pylori, a well-established class I carcinogen, remains the most prominent microbial risk factor for gastric cancer. However, emerging studies indicate that alterations in the broader gastric and intestinal microbial communities, referred to as dysbiosis, may also contribute to tumor initiation, progression, and immune evasion. These microbial shifts can lead to chronic inflammation, genotoxic metabolite production, and modulation of signaling pathways such as NF-κB and Wnt/β-catenin. This review explores the current understanding of the gut microbiome’s contribution to gastric cancer pathogenesis, including microbial signatures associated with precancerous lesions and the tumor microenvironment. Furthermore, the potential of microbiota-based biomarkers and therapeutic interventions, including probiotics, prebiotics, and fecal microbiota transplantation, is discussed as part of emerging precision medicine strategies.

A woman in her early 40s with MLH1-deficient Lynch syndrome was incidentally found to have a cecal gut-associated lymphoid tissue (GALT)/dome carcinoma during routine surveillance colonoscopy. This case highlights the co-occurrence of 2 rare entities: a germline MLH1 pathogenic variant and a GALT/dome carcinoma, now recognized within the lymphoglandular complex-like carcinoma spectrum, which carries potential for nodal metastasis. The intersection of mismatch repair deficiency and GALT/dome carcinoma raises a management dilemma: prophylactic colectomy vs endoscopic surveillance in the absence of high-risk histologic features. We review the literature to guide management in this rare scenario.