Although the three missense mutations in GCNT2 have a benign effect, a possibility exists that the candidate genes (GCNT2, HSF4 and CRYAA) might harbour mutations that are responsible for total congenital cataract.

Although deleterious effects of the three amino acid substitutions were not evaluated, one substitution of GLDC gene (S44R) could be disease-causing because of its drastic amino acid change, affecting amino acids conserved in different primate species. This study confirms the diagnosis of NKH for the first time in vervet monkeys with cataracts.

Advances in molecular techniques have shown that genetic factors predispose individuals to cardiovascular diseases (CVD). These techniques have made it possible to identify disease-causing genes, prediction to disease susceptibility and responsiveness to drug interventions. For the purpose of this review, therapeutic intervention (niacin) was conducted in a nonhuman primate model to assess the impact of six coincident single nucleotide polymorphisms (cSNP) identiied in prioritised reverse cholesterol transport (RCT) and high-density lipoprotein (HDL) metabolism genes. Gene expression indings conirmed that these genetic variants may have a direct impact on the RCT pathway and drug intervention (niacin) response.