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It has come to the authors’ attention that the H. pylori P12ΔrfaD mutant described in this paper is in fact a double mutant for P12ΔrfaE/ΔrfaD. The kanamycin cassette used to replace the gene 0859 (rfaD) also disrupts the starting methionine of the gene 0858 (rfaE). The loss of the rfaE gene explains the observed phenotype, that is, lack of NF‐κB activation after H. pylori infection (shown in Figure 4B), despite an intact type IV secretion system able to translocate CagA (shown in the Supplementary Figure 5B).