Helicobacter pylori (Hp) employs a multi-component type IV secretion system (T4SS) to secrete the effector protein CagA into the cytosol of infected host cells. A longstanding challenge has been to identify the host cell receptor(s) involved. Two recent studies have independently unveiled human beta(1) integrin as the receptor but are divided over which T4SS proteins bind to beta(1) integrin. Here we revisit the two models in light of previous findings and recent progress in the field. More concerted efforts are required to fully understand the complex T4SS mechanisms that underpin Hp pathogenesis.