This study analyzed 95 non-synonymous single nucleotide polymorphisms (nsSNPs) in the human FXN gene, which codes for the frataxin protein involved in Friedreich's ataxia. Eight computational tools were used to evaluate the potential effects of the nsSNPs on frataxin protein stability and activity. Molecular dynamics simulations were performed on the native and mutant frataxin protein structures over time to analyze structural and functional changes from the nsSNPs. The results of this computational analysis of the nsSNPs could provide insight into how functional nsSNPs may contribute to causing Friedreich's ataxia.