In an attempt to clarify the potential connections/interplay among these interrelated factors, we performed a series of in vitro experiments on coculture between EGCs and intestinal epithelial cells treated with PA (the major source of fat in the hypercaloric diet) and LPS (a well‐recognized activator of the first step of NLRP3 signaling and an index of endotoxemia associated with HFD intake). The gene discussed is NLRP3; the disease is serum lipopolysaccharide activity.