NAT2 and tuberculosis: Isoniazid, which is widely used in the treatment and prevention of tuberculosis, inactivates CYP2A6 via irreversible suicide inhibition.6 When co-administered, efavirenz concentrations in CYP2B6 slow metabolisers are further increased by isoniazid’s inhibition of CYP2A6.7,8,9 Polymorphisms in the NAT2 gene that confer slow NAT2 acetylator genotypes and increase isoniazid exposure, further increase efavirenz concentrations.10,11,12