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Mallory-Denk bodies (MDBs), also called "Mallory bodies," are cytoplasmic hyaline inclusions found in hepatocytes. Initially considered specific to alcohol-related steatohepatitis (ASH), MDBs also appear in metabolic dysfunction-associated steatohepatitis (MASH, formerly nonalcoholic steatohepatitis or NASH), cholestatic liver diseases, primary biliary cirrhosis (PBC), and hepatocellular carcinoma (HCC).[1][2] In 1911, Frank Burr Mallory identified these histological structures in the hepatocytes of patients with alcoholic hepatitis. In 1975, Helmut Denk established the first animal model by administering griseofulvin to mice, prompting the shift from the term "Mallory bodies" to "Mallory-Denk bodies" (see Image. Mallory-Denk Bodies).[3] Human studies subsequently revealed that MDBs primarily consist of keratins, molecular chaperones, cotransporters, and additional aggregated proteins. Histologically, clinicians classify MDBs into subtypes—classic, nonkeratinous, rounded, and variants—to guide grading and staging during liver biopsy evaluation. MDB formation reflects cellular stress and dysregulated cell cycle control, which impairs hepatocyte regeneration and affects other proliferating cell types. Since cell cycle dysregulation is central to the liver pathologies listed above, MDBs serve as a histological marker with clinical relevance. In the early stages of inflammation, MDB formation may offer protective effects by limiting damage and delaying the progression of fibrosis. However, persistent or compounded stressors can worsen disease severity. The learning activity below explores the molecular pathways underlying MDB formation, the triggers that induce their development, and evidence-based associations with clinical outcomes. Interprofessional teams, including primary care, gastroenterology, and pathology, contribute to disease staging and management. Students in these fields become familiar with MDB morphology as part of their histopathological training.