Given the role of ALPK1 in the regulation of the NF-κB pathway in infection, we next asked if the ALPK1 p.V1092A variant could activate NF-κB signaling and thus substitute for mutation of CYLD. To do this, we generated full-length ALPK1 wild-type and p.V1092A mutant cDNA constructs in an expression vector. This evidence concerns the gene NFKB1 and infection.