During infection, K8 and/or K18 were previously shown to assist toxin internalization (Nava-Acosta and Navarro-Garcia, 2013), to favor intracellular pathogen replication (Claser et al., 2008) and to allow stable pathogen docking to the host cell surface (Carlson et al., 2002; Batchelor et al., 2004; Russo et al., 2016). Here, KRT8 is linked to infection.