In the 1960s, Jeff Watkins and colleagues discovered N-methyl-d-aspartate (NMDA) receptors, and since then, it has been a pharmacodynamic target for many neurological and psychiatric drugs. NMDA is a glutamate receptor and ion channel protein located in nerve cells. There are many subunits for the NMDA receptor. They are all working together in a harmonic pattern to regulate the calcium permeability and the voltage-dependent sensitivity to magnesium influenced by the binding of glutamate as a neurotransmitter. In this paper, a light will be shed on glutamate ionotropic receptor NMDA subunits. There are several names for the GRIN gene, such as GluN. It is proven that GRIN has a significant influence on memory and learning abilities. Interestingly, part of how GRIN executes its function by interacting with other receptors. For example, GRIN counteracts the role of the cAMP response element-binding protein (CREP) receptor, while its function modulated by dopamine D1 receptors. Therefore, Hypo-functioning and mutation of this gene play a pivotal role in developing neurodevelopmental disorders wither it was with or without hyperkinetic movements and with and without seizures, besides several psychotic disorders such as schizophrenia. Hence, NMDA receptors subunits have been a target for therapeutic development for the last years. With the advancements in the genetic and genomic science, investigators are trying to find the alternative splicing of GRIN, understanding location and the distribution of NMDA subunits with deeper lucidity than it is currently. However, that is faced by some challenges. Modifying the NMDA receptor subunits to treat one condition can lead to potential harm effect in another condition because, sometimes, NMDA works complicatedly inversely with many other receptors and neurotransmitters, which will have an impact on the investigators to find the appropriate way to cause no harm.