TRIM32 is an E3 ubiquitin ligase with multifunctional roles in skeletal muscle maintenance, autophagy regulation, and immune responses 1. As an E3 ubiquitin ligase, TRIM32 mediates ubiquitination of diverse substrates including STIM1, regulating protein stability and cellular signaling 2. TRIM32 participates in autophagy regulation by facilitating autophagosome assembly and maturation, contributing to selective clearance of pathogens and damaged organelles 34. In cancer biology, CDK2-phosphorylated TRIM32 translocates to the nucleus where it inhibits TC45-mediated STAT3 dephosphorylation, promoting radioresistance in triple-negative breast cancer 5. Genetically, TRIM32 variants cause limb-girdle muscular dystrophy type 2H (LGMD2H), characterized by skeletal muscle dystrophy, myopathy, and atrophy, with pathogenic variants occurring primarily in C-terminal NHL repeats 16. TRIM32 is also associated with Bardet-Biedl syndrome 11. Despite TRIM32's broad tissue expression, LGMD2H predominantly affects skeletal muscle, indicating tissue-specific functional importance 1. The protein's roles extend to regulating cell cycle progression, NF-κB signaling, and cellular stress responses, making TRIM32 a critical regulator of both physiological and pathophysiological processes.