SRC and infection: Although Src inactivation leads to the dephosphorylation of other Src substrates, such as vinculin, cortactin and ezrin [45,48,49], the tyrosine phosphorylation of CagA is maintained by Abl kinases in late phase infections [6,7], ensuring that CagAPY constitutively stimulates signaling pathways in host cells (Fig. 2B).