After Helicobacter pylori enters the stomach, three steps are vital for infection: (i) establishing colonization; (ii) evading host immunity; and (iii) invading gastric mucosa; the last step is what is associated with diverse outcomes. Urease activity and motility mediated by the flagella of H. pylori are important in harboring colonies beneath the gastric mucus in niches adjacent to the epithelium. Several putative adhesins attach the organism to the gastric epithelium and prompt the succeeding processes for evading host immunity and invading the mucosa. Successful colonization is thus the leading and critical step. From another point of view, this can be a novel target to control this common and important infection. This review summarizes the putative adhesins that influence the evasion of host immunity, and how these could determine different clinico-pathologic outcomes. The putative adhesins include the interplay between bacterial and host Lewis antigens (type I: Le(a) and Le(b); type II: Le(x) and Le(y)), the dominant pathway between BabA and Le(b), the SabA adhesin binding to sialylated Le(x) that is upregulated in inflamed gastric tissue or those with weak-Le(b), the CagL apparatus to adapt with the alpha5beta1 integrin to mediate a type IV secretory system for CagA translocation into the epithelium; and other outer membrane proteins as HopZ, AlpA/AlpB, or OipA, without known corresponding receptors. This review implicates the adhesins vital for bugs that could be alternatively provided as novel targets for us to overcome the colonization.