CYP2C9*6 is assigned no function based on strong supporting evidence in heterozygous and homozygous patients. This allele was first identified in a CYP2C9*6/*6 patient experiencing phenytoin toxicity after recently starting the medication. Based on serial phenytoin plasma concentrations after discontinuing phenytoin, the patient had an estimated 17% phenytoin clearance compared to wildtype (11740344). In a separate case report, a patient with CYP2C9*6/*6 genotype stable on a low weekly warfarin dose demonstrated impaired warfarin metabolism with an S:R warfarin ratio 6x greater than expected (15094935). The S:R warfarin ratio of this patient was the highest among 52 patients on a stable dose of warfarin with a CYP2C9 genotype of *1/*1, *1/*2, *1/*3, *2/*2, or *2/*3 (17895500). Two subjects (CYP2C9*1/*6 and CYP2C9*5/*6 genotype, respectively) had decreased losartan metabolism compared to wildtype subjects based on urinary metabolites after a single 25mg dose (15289788). Three CYP2C9*1/*6 subjects and one CYP2C9*5/*6 subjects had lower phenytoin metabolism compared to wildtype based on urinary excretion of a phenytoin metabolite after a single 300mg dose. Additionally, the CYP2C9*5/*6 subject demonstrated the lowest phenytoin metabolism as the only subject of the 109 subject cohort to have a urinary metabolite concentration below the limit of quantification (16220110). CYP2C9*6 is defined by a deletion resulting in a frameshift and not included in in vitro studies as it is it is a null allele resulting in no protein formation (23752738). Although one CYP2C9*1/*6 subject had a similar acenocoumarol metabolite plasma concentration compared to wildtype subjects 8 and 24 hours after a single 8mg dose (21811894), the experts did not deem this result as convincing conflicting evidence based on the small sample size. Therefore, consensus among experts was no function with an activity value of 0 based on strong evidence.