TO THE EDITOR: Helicobacter pylori (H. pylori) is one of the most common bacterial infection in the world and has been associated with various gastroduodenal pathologies, from gastritis to gastric malignancies. Cure of infection has become the core of ulcer therapy, and it has been suggested that eradication could play a role even in the management of other diseases, both involving the GI tract (e.g., nonulcer dyspepsia or MALT lymphoma) (1) and not involving it (e.g., headache, Raynaud phenomenon) (2). In vivo, H. pylori eradication has turned out to be very demanding, possibly because of several different factors (e.g., peculiar echological niche, development of antibiotic resistance, components of therapeutic regimens, dosing frequency, treatment duration, and poor patient compliance (3). Currently the preferred way to cure the infection is a regimen of profound gastric acid suppression combined with two antibiotics, usually chosen among amoxycillin, clarithromycin, tetracycline, or imidazole (4). Unfortunately, patients who fail eradication after a first course of therapy are not a rarity. Similarly to other bacterial infection, the management of noncured patients can be demanding, and patients are likely to receive repeated treatments, each time with different antimicrobials, on the often unproved assumption of H. pylori resistance to the drugs first employed. This policy of exposing patients to many different drugs increases the possibility of the appearance of multiresistant strains and of adverse effects. Analysis of chemiosusceptibility shows that a variable proportion of noneradicated patients is made of subjects who have been compliant with the therapeutic regimen and who harbor strains sensible to the administered drugs (5). In these patients, the reason(s) for treatment failure is/are unclear, and it is possible that a different treatment duration and/or drag dosage could eventually lead to eradication.