Small intestinal bacterial overgrowth (SIBO) manifests with a variety of gastrointestinal symptoms, including bloating, flatulence, abdominal pain, nausea, dyspepsia, fatigue, diarrhea, and constipation [1]. SIBO has been implicated as a cause of hepatic encephalopathy and of d-lactic acidosis in patients with short bowel syndrome [2,3]. Moreover, SIBO is associated with a variety of conditions outside of the gastrointestinal system, including rosacea [4], restless legs syndrome [5], interstitial cystitis [6], and chronic prostatitis [7], and correlates with the level of somatic pain in fibromyalgia [8]. Along these lines, recent studies have reported a link between SIBO and cardiovascular disease.Ponziani et al. [9] recently published data linking SIBO with subclinical atherosclerosis through the vitamin K-dependent activity of the matrix GIa-protein (MGP), which maintains arterial structure and function through prevention of calcification of vessel walls and the regulation of the extracellular matrix. MGP is carboxylated by the cofactor vitamin K2 to assume its active form. Increased expression of the inactive, uncarboxylated MGP is a marker of low vitamin K2 status, associated with signs of early vascular disease such as arterial stiffness and vascular calcifications, as well as cardiovascular morbidity and mortality. The bulk of vitamin K2 in humans is derived from gut bacterial biosynthesis, and prior studies showed low circulating levels of vitamin K2 in patients with SIBO [10].In their prospective cohort study, 39 patients were included with SIBO suspected on the basis of gastrointestinal symptoms who also had low cardiovascular disease risk and no prior history of cardiovascular events. All patients underwent a glucose breath test, and 12 (39.0%) were diagnosed with SIBO. The median level of inactive MGP was significantly increased among patients with SIBO compared to patients without SIBO (9.5 vs 4.2 µg/L, p = 0.02). Correspondingly, arterial pulse wave velocity, which increases when there is an increase in arterial stiffness, was increased among patients with SIBO compared to that observed in the group without SIBO (10.25 vs 7.68 m/s, p = 0.002). The authors concluded, then, that SIBO is associated with reduced MGP activation as well as arterial stiffening, regarded as important indicators of subclinical atherosclerosis [9].In the current issue of Digestive Diseases and Sciences, Fialho et al. [11] expand upon this work by demonstrating a previously undescribed association between SIBO and coronary artery disease (CAD). In their study, they retrospectively reviewed medical records at a single tertiary care center in order to identify all patients who underwent a glucose hydrogen/methane breath test. Records were crossreferenced to identify 160 patients who had undergone left heart catheterization with coronary angiography at the same center. These records were reviewed to determine the presence and extent of CAD. Importantly, widely recognized risk factors for CAD such as age, smoking, diabetes, hypert...