*2.1. Study Population*

The institutional review board of the Lebanese University approved the recruitment procedure and the genetic protocols (2182/28, on 16 December 2015). This cross-sectional study involved 460 unrelated Lebanese participants who were apparently healthy (free of chronic diseases; cardiovascular or cancer) individuals.

#### *2.2. Clinical and Biological Data Collection*

All measurements, including demographic, clinical, and biochemical measurements, were assessed as described previously [11]. Nuclear DNA was extracted from whole-blood samples according to the manufacturer's recommendations (QIAamp DNA blood mini kit, Qiagen, Hilden, Germany). Very briefly, 4 μg of total DNA from 200 μL of whole human blood was extracted through lysis and continuous spinning. A KASP genotyping assay (LGC group, Berlin, Germany) was used to genotype rs2569190A>G in *CD14*. Hypercholesterolemia was defined as an elevation of total cholesterol (Tchol) and/or low-density cholesterol (LDL-C) levels. Tchol and LDL-C were considered high if their values were ≥150 and ≥100 mg/dL, respectively. High-density cholesterol (HDL-C) levels were considered low if their values were ≤50 and ≤40 mg/dL in females and males, respectively. HTN was defined as systolic blood pressure ≥130 mmHg or diastolic ≥85 mmHg.

## *2.3. Statistical Analyses*

SPSS statistical software version 24.0 [12] was used to perform all our statistical analyses except the power analysis. GPower 3.1.9.4 software [13] was used for the power analysis. Continuous variables were presented as mean value ± standard deviation, and categorical ones were shown as numbers and percentages. A chi-squared goodness-of-fit test was performed to determine if the genotypes of rs2569190A>G in *CD14* were in Hardy–Weinberg equilibrium (HWE).

To study the association between rs2569190A>G in *CD14* and hypercholesterolemia and HTN, a multivariate logistic regression model was used while correcting for di fferent confounding factors (age, gender, body mass index, marital status, smoking, and physical activity). This analysis was performed under the assumption of additive (AA vs. GA vs. GG) and recessive models (AA and GA vs. GG). The sample size needed to reach a statistical power of at least 0.90 in a two-sided test with α = 0.05 and an e ffect size of 0.2 was 409 individuals.
