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“Quantile-dependent expressivity” is a dependence of genetic effects on whether the phenotype (e.g., triglycerides) is high or low relative to its distribution in the population. Quantile-specific offspring-parent regression slopes (β OP ) were estimated by quantile regression for 6227 offspring-parent pairs. Quantile-specific heritability ( h  2 ), estimated by 2β OP /(1 + r spouse ), decreased 0.0047 ± 0.0007 (P = 2.9 × 10 −14 ) for each one-percent decrement in fasting triglyceride concentrations, i.e.,  h  2  ± SE were: 0.428 ± 0.059, 0.230 ± 0.030, 0.111 ± 0.015, 0.050 ± 0.016, and 0.033 ± 0.010 at the 90th, 75th, 50th, 25th, and 10th percentiles of the triglyceride distribution, respectively. Consistent with quantile-dependent expressivity, 11 drug studies report smaller genotype differences at lower (post-treatment) than higher (pre-treatment) triglyceride concentrations. This meant genotype-specific triglyceride changes could not move in parallel when triglycerides were decreased pharmacologically, so that subtracting pre-treatment from post-treatment triglyceride levels necessarily created a greater triglyceride decrease for the genotype with a higher pre-treatment value (purported precision-medicine genetic markers). In addition, sixty-five purported gene-environment interactions were found to be potentially attributable to triglyceride’s quantile-dependent expressivity, including gene-adiposity ( APOA5 ,  APOB ,  APOE ,  GCKR ,  IRS-1 ,  LPL ,  MTHFR ,  PCSK9, PNPLA3, PPARγ 2), gene-exercise ( APOA1, APOA 2 , LPL ), gene-diet ( APOA5, APOE, INSIG 2 , LPL, MYB, NXPH1, PER 2 , TNFA ), gene-alcohol ( ALDH 2 , APOA5, APOC3, CETP, LPL) , gene-smoking ( APOC3, CYBA, LPL, USF1) , gene-pregnancy ( LPL ), and gene-insulin resistance interactions ( APOE ,  LPL) .

Gene-environment interactions due to quantile-specific heritability of triglyceride and VLDL concentrations