At baseline (0 h), FH compared with control subjects had significantly lower expression of genes involved in fatty acid metabolism (ACACA, CPT1A and FADS1), cholesterol biosynthesis (FDPS), the gene coding for the scavenger receptor MSR1 and genes involved in the transcription of lipid genes (NR1H3 and SREBF2) (0·001 ≤ P ≤ 0·02) (Supplementary Table S1). The gene discussed is SREBF2; the disease is familial hyperaldosteronism.