In the neonatal model of infection with the apicomplexan parasite, Cryptosporidium parvum, we showed that increased permeability was the result of both the parasite on the adherens junctions proteins E-cadherin and β-catenin and the release of inflammatory cytokines (TNFα and IL1β) by inflammatory monocytes (De Sablet et al., 2016). This evidence concerns the gene CDH1 and infection.