Deiodinases, homodimeric thioredoxin fold-containing selenoproteins, and thyroid hormone signalling are specialised in a time- and cell-specific manner by these proteins. This guarantees sufficient T3 activity in growing tissues, healthy individuals, and a variety of disease situations. By transforming the prohormone T4 into T3, the physiologically active thyroid hormone, D2 activates thyroid hormone. D2 expression is tightly controlled by transcriptional mechanisms that are activated by both endogenous and exogenous stimuli. Moreover, there is a catalytically-activated on/off switch mechanism for D2 activity that works with D2 ubiquitination and deubiquitination. T4 and T3 molecules are both rendered inactive by D3, which stops the thyroid hormone's function. Deiodinases influence the intracellular levels of T3, which in turn affects gene expression on a cellspecific basis, and so play a role in thyroid hormone homeostasis, development, growth, and metabolic control. With coordinated reciprocal alterations in D2-mediated thyroid hormone activation and D3-mediated thyroid hormone inactivation, tight regulation of these pathways by T3 is frequently attained. Here, we investigated the impact of a local increase in thyroid hormone action in the brain caused by a DIO3 deficit on social behaviours. Dio3 -/- mice of both sexes showed a significant increase in aggression-related behaviours and minor abnormalities in olfactory function, despite the fact that we did not notice changes in friendliness.