Moreover, the significant effects of both Poly I:C and SGAs on adipokines (leptin and adiponectin) and locomotor activity, with SGA-driven changes in insulin and prolactin, indicate that altered locomotion and divergent endocrine modulation serve as candidate pathways contributing to NDD-related metabolic risk.<h4>Discussion</h4>These results highlight that NDD-related locomotor and endocrine changes should be considered as potential biological factors when finding effective strategies for preventing metabolic events during SGAs medication. The gene discussed is INS; the disease is Neurodevelopmental delay.