Recently, excess lipid deposits in NAFLD were reported to upregulate NLRC4 expression, a crucial component of the inflammasome, via activating TLR4 in tumor-associated macrophages in the liver, promoting their polarization towards M2 and enhancing IL-1β and VEGF production to favor the growth of metastatic CRC cells [10]. This evidence concerns the gene TLR4 and metabolic dysfunction-associated steatotic liver disease.