Immortal time bias or sorafenib effect in elderly patients with HCC?

carcinoma in patients carrying the Z allele. While intriguing, the hypothesis raised by Ponzetto et al. remains highly speculative. Although Shimoda et al. found that CagA is present in serum-derived exosomes of patients infected with H. pylori, it is unknown whether these exosomes are released in sufficient amount to be taken up by hepatocytes and efficiently activate the c-Jun N-terminal kinase and c-Jun pathway. Moreover, activation of c-Jun by CagA has been observed in gastric epithelial cells exposed to H. pylori, and whether CagA can activate the c-Jun N-terminal kinase and c-Jun also in hepatocytes has to be shown. Co-occurrence of peptic ulcer by H. pylori has been observed in patients with alpha1-antitrypsin deficiency. However, whether infection with H. pylori is associated with a higher rate of liver disease in patients with alpha1-antitrypsin deficiency has not been investigated so far. In summary, extensive studies both in preclinical models and in the clinic are needed to show whether H. pylori is indeed a modifier of the expressivity of liver disease in alpha1-antitrypsin deficiency.