Ito 2006.

Methods	Setting: first visit at Aichi Cancer Center Hospital (ACCH), Japan Recruitment: screening of first‐visit outpatients (whether consecutive or not is unknown)
Participants	697 included out of 859 eligible smokers. Smoker defined as smoking at least 1 cigarette on the previous day. Mean age 46.5, 40.5% female, mean cpd: 22.2, pre‐contemplator/contemplator: 70% Therapist: trained interviewer
Interventions	Intervention: information at baseline on the effect of L‐myc polymorphism on modulating the risk of cancer due to smoking (5 to 10 minutes). Sent genotype report at 3 months, with same information about effect of polymorphism (65% got genotype information) Control: just followed‐up for smoking status
Outcomes	Definition of abstinence: point prevalence at 9 months (continuous abstinence, not smoking at both the 3‐ and 9‐month follow‐ups also reported, but genotype only provided after 3 months follow‐up) Duration of follow‐up: 9 months Biochemical validation of non‐smokers: none (attempt made but none agreed to return for CO measurement)
Identification
Notes	Not given genotype until 3 months. Most participants in both groups had already quit at 3 months, small proportion of new quitters after 3 months. Source of funding: This work was supported in part by a Grant‐in‐Aid for Cancer Research from the Japanese Ministry of Health, Labor and Welfare (17‐1).
Risk of bias
Bias	Authors' judgement	Support for judgement
Random sequence generation (selection bias)	High risk	Pseudo‐random allocation by week of attendance
Allocation concealment (selection bias)	High risk	Allocation known at time of enrolment, so potential for selection bias
Blinding of outcome assessment (detection bias) All outcomes	Low risk	Outcomes assessed by postal questionnaire, biochemical validation attempted but refused. Similar amount of contact between groups
Incomplete outcome data (attrition bias) All outcomes	Low risk	Complete data for 52.9% (369), did not differ significantly between groups