Previous studies using the apolipoprotein E (ApoE) knockout (ApoE−/−) model of atherosclerosis demonstrate that inhibition of TMA lyase via oral administration of the choline structural analogs 3,3-dimethyl-1-butanol (DMB) or fluoromethylcholine (FMC) is beneficial, such that mice given these inhibitors have reduced circulating TMAO levels coupled with reductions in endogenous macrophage foam cell and atherosclerotic lesion formations [26, 27]. The gene discussed is APOE; the disease is atherosclerosis.