In hyperthyroidism, there is a significant decrease in the level of OPA1 and Sam50 and selective hyperactivation of the MIC60 subcomplex while maintaining the stability of the MIC10 subcomplex, which creates a functional imbalance, disrupts cristae architecture, and critically impacts energy metabolism and Ca2+ homeostasis in the liver mitochondria of animals with this pathology (Figure 7). This evidence concerns the gene SAMM50 and hyperthyroidism.