​Research has shown that unique African genetic variants in hepatic metabolism genes alter the efficiency of drug metabolism and, thus, drug response. For example, CYP2D6, an important enzyme from the cytochrome P450 superfamily for drug metabolism, assists in the formation of endoxifen from tamoxifen in breast cancer, and metabolism of primaquine to 5-hydroxyprimaquine in malaria and pneumocystis pneumonia.​

The African-specific CYP2D6*17 allele causes a reduced function on the CYP2D6 enzyme and decreases substrate affinity, thus negating pharmaceutical benefits for a portion of African patients. Numerous methods have been employed to study such effects in a physiologically relevant in-vitro model. Primary human hepatocytes, for example, are the current gold standard but are expensive and difficult to maintain for long periods in culture.​

Cancer-derived cell lines, such as HepG2s, are chromosomally inaccurate and lack the maturity required for physiologically relevant metabolism. In the bioengineering and integrated genomics group lab, researchers have developed an induced pluripotent stem cell-derived 3D liver model.​

This inexpensive model can be genetically engineered to compare the effect of African genetic variants with classical European screening trials on frequently prescribed pharmaceutical compounds used in treating high-impact diseases in South Africa.​

Importantly, this research model can be applied across a range of diseases, from infectious diseases to cancer to the much-needed and under studied mental health pathologies.​