This may be a direct effect of infection, as Helicobacter activates NF-κB via chronic inflammation and the activation of interleukins, such as IL-4 (Lee et al, 2005), or in response to lipopolysaccharides (Hynes et al, 2004) and NF-κB in turn is able to activate Shh (Nakashima et al, 2006). This evidence concerns the gene IL4 and infection.