Chronic mental illnesses are persistent and disrupt cognition, emotion regulation and behaviour, and their exact causes and mechanisms remain largely unknown. Previous studies identified several genetic factors that play a role in their development. Nuclear Distribution Element 1 (NDE1) and Nuclear Distribution Element-Like 1 (NDEL1) are proteins that arise form a gene duplication event and are vital in cell mitosis and neurodevelopment. They have been associated with brain malformations and neurodevelopmental disorders. Although being structurally similar, they exhibit distinct pathophysiological functions. Rare codon bias is a tendency for some codons to be more frequently used than others in a specific species, while they encode for the same amino acid. Codon rarity has been demonstrated to affect translation speed, protein folding, translational control, and protein expression levels in multiple known genomes. In human NDE1 and NDEL1 genes, the latter shows an increase in frequency of rare codon usage. In this thesis, I first investigated whether the difference in codon rarity between NDE1 and NDEL1 was conserved across multiple species that represented major vertebrate genera. Next, I explored if altering the codons responsible for encoding NDE1 and NDEL1 could mitigate the differences in expression levels between these two proteins. To achieve this, I examined NDE1 constructs that used codons closely, matching ones found in NDEL1, while maintaining the correct amino acid sequence, and vice versa. Finally, I examined the expression patterns of both wild type and switched codon NDE1 and NDEL1 proteins by fluorescent microscopy with the aim of identifying any noticeable distinctions if such differences existed. The preference of NDEL1 for rare codon usage that had previously been seen in humans, was also seen in non-human primates and non-primate mammals, suggesting the rare codon bias differences between the two genes to be conserved across mammalian species. Our findings indicated that the difference in codon rarity in wild type NDE1 and NDEL1 had an impact on their respective expression levels, with NDE1 exhibiting higher expression within cells. Notably, when examining constructs with switched codons, there was indication of this difference being nullified. This observation suggests that the use of more commonly occurring codons could potentially reverse the trend of lower protein expression levels and that rare codon bias may be partially responsible for the differing functions of the two proteins.