Following these events, CagA interacts with various host signaling factors and triggers cancer-related pathways that can be broken up into two categories, those that depend on tyrosine phosphorylation of the EPIYA motif [SHP-2, C-terminal Src kinase (CSK), Crk, E-cadherin] and those that depend on CagA, but are phosphorylation-independent (Grb2, c-Met, Par-1b/MARK2, ZO-1) (see below). The gene discussed is MARK2; the disease is cancer.