In patients harboring LGMD2H-causing TRIM32 variants, defects in the E3 ubiquitin ligase activity of TRIM32 induce premature senescence of satellite cells, insufficient terminal differentiation, and defective autophagy, which results in delayed or impaired myogenesis, skeletal muscle atrophy, various muscle symptoms, ultimately causing difficulties in daily life without other people’s help or aid. The gene discussed is TRIM32; the disease is autosomal recessive limb-girdle muscular dystrophy type 2H.