Skeletal muscle toxicity is the primary adverse effect for statins. In this review, we summarize current knowledge regarding the genetic and non-genetic determinants of risk for statin induced myopathy. Many genetic factors were initially identified through candidate-gene association studies (CGAS) limited to pharmacokinetic (PK) targets. Through genome-wide association studies (GWAS), it has become clear that SLCO1B1 is among the strongest PK predictors of myopathy risk. GWAS have also expanded our understanding of pharmacodynamic (PD) candidate genes, including RYR2. It is anticipated that deep re-sequencing efforts will define new loci with rare variants that contribute as well, and sophisticated computational approaches will be needed to characterize gene-gene (GxG) and gene-environment (GxE) interactions. Beyond environment, race is a critical covariate, and its influence is only partly explained by geographic differences in the frequency of known PD and PK variants. As such, admixture analyses will be essential to a full understanding of statin-induced myopathy.