While these data could be explained by a transcriptional control of TLR4 by wild-type p53, as previously suggested by Menendez et al. [27], we did not observe the same correlation in other tumor contexts known to have no or low bacterial load (such as breast and liver cancers) or with a lower abundance of Gram-negative bacteria (such as lung cancer) [28] (Supplementary Fig. S3a, b). The gene discussed is TP53; the disease is neoplasm.