Commentary: reporting and assessing evidence for interaction: why, when and how?

gene-by-environment interaction studies: revelations and remedies. Epidemiology 2011;22:400–07. 4 Weinberg CR, Shi M, Umbach DM. A sibling-augmented case-only design for assessing multiplicative gene-environment interaction. Am J Epidemiol 2011;174:1183–89. 5 Kistner EO, Shi M, Weinberg CR. Using cases and parents to study multiplicative gene-by-environment interaction. Am J Epidemiol 2009;170:393–400. 6 Umbach DM, Weinberg CR. The use of case-parent triads to study joint effects of genotype and exposure. Am J Hum Genet 2000;66:251–61. 7 Lin PI, Vance PM, Pericak-Vance MA, Martin ER. No gene is an island: the flip-flop phenomenon. Am J Hum Genet 2007;80:531–38. 8 Shi M, Weinberg CR. How much are we missing in SNP-by-SNP analyses of GWAS? Epidemiology 2011;22: 845–47. 9 Weinberg CR. Applicability of the simple independent action model to epidemiologic studies involving two factors and a dichotomous outcome. Am J Epidemiol 1986; 123:162–73. 10 Weinberg CR. Interaction and exposure modification: are we asking the right questions? Am J Epidemiol 2012; doi:10.1093/aje/kwr495. 11 Finney DJ. Probit Analysis. 3rd edn. New York: Cambridge University Press, 1971. 12 Siemiatycki J, Thomas D. Bological models and statistical interactions: an example from multistage carcinogenesis. Int J Epidemiol 1981;10:383–87. 13 Wacholder S, Han S, Weinberg C. Inference from a multiplicative model of joint genetic effects on ovariance cancer risk. J Natl Cancer Inst 2011;103:82–83.