In addition, with the possibility that some monocytes infiltrating the liver in NAFLD/NASH may give rise to infRes-KCs (Figure 3), this brings into question the strategy to target all recruited cells in NAFLD through CCL2 inhibitors (60), as potentially infRes-KCs and Temp-macs may play distinct roles in disease pathology. Here, CCL2 is linked to metabolic dysfunction-associated steatotic liver disease.