These results support the hypothesis proposed by Morton et al. that cholesterol presence and an organized bilayer membrane structure are critical for enabling TNF-TNFR1 clusters to undergo necessary conformational changes, thus initiating downstream signaling in macrophages.41 Furthermore, we found that infection with WT or PldA-in H. pylori disrupts membrane fluidity, which prevents the ubiquitination of RIP1. Here, TNFRSF1A is linked to infection.