Furthermore, the association between GML and gastric carcinogenesis is also supported by data coming from more fundamental studies, showing that both processes (lymphomagenesis and carcinogenesis) share some common mechanisms, and in particular, the lymphocyte T stimulation, induced by H. pylori, the same pathogen involved in both GML and gastric adenocarcinoma pathogenesis, with an excessive TH1 pro-inflammatory immune response likely responsible for the evolution towards these two diseases [127,128]. Here, GML is linked to gastric adenocarcinoma.