Our results indicate that the use of thyroxine as an adjunctive therapy for depression may normalize neurotransmission not only by acting on neurons, as other authors suggest [13,25], but also by influencing the function of astrocytes and microglial cells, weakening disturbances in the glycolysis process and possibly also by reducing expression of the active form of caspase-1 to regulate the process of neuroinflammation, but this potential effect requires further research. This evidence concerns the gene CASP1 and depressive disorder.