Intellectual Disability (ID) is a complex neurodevelopmental disorder characterized by significant limitations in intellectual functioning, adaptive behavior, and the presence of incomplete or arrested mental development. Genetic factors, neurophysiological or environmental factors, various traumas or a combination of all these factors may be effective in the etiology of ID. Genetic factors such as mutations, deletions, variations, and rearrangements in genes encoding proteins may play an important role in brain development and cognitive function. Environmental factors that play an important role in neuroinflammation may affect synaptic function. Thus, immunological dysfunctions may occur. In addition, inflammatory events may develop as a result of infection developing in the prenatal period. The inflammatory event is associated with long-term consequences related to behavior and cognition. Thus, the susceptibility to cognitive and behavioral disorders increases. Cytokines play an important role in the molecular and cellular mechanisms associated with cognitive processes in the central nervous system. Cytokine imbalances occur as a result of the absence or overexpression of cytokines. These imbalances affect hippocampal-dependent memory forms and synaptic plasticity. In addition, the interaction of many cytokines in the immune system has been reported, and imbalances that occur in multiple interactions of cytokines can lead to various neurodevelopmental disorders. Interleukins are important cytokines and imbalances in interleukin levels have been associated with genetic variations in intron, coding or promoter regions. It is thought that functional interleukin gene variations may be effective in the development of ID. Therefore, in this chapter, we aimed to examine interleukin gene variations that may be important in evaluating the possible effects of interleukin on ID disorder associated with cognitive function development.