Although it can not be excluded that the relative expression levels and E3 ligase activities of secreted SopA and host TRIM56 and TRIM65 in vivo determine the outcome of this host–pathogen targeting event and account for the discrepancy in presented findings and previous data, our observations in cultured epithelial cells indicate a progressive decay of endogenous TRIM56 and TRIM65 protein levels upon standard Salmonella infection conditions. The gene discussed is TRIM65; the disease is Salmonella Infections.