ENA78 was recently shown to be upregulated during the genesis of HCC.35 In addition, eotaxin was lately revealed to be elevated in the development of MASLD and inhibition of eotaxin attenuated disease progression.36 Likewise, RANTES promotes liver-neutrophilic infiltration leading to MASH and HCC progression, whereas neutralization of RANTES attenuates hepatocarcinogenesis in a murine model.37 All three chemokines (RANTES, eotaxin, and ENA78) promote vascular inflammation and atherogenesis.38–40. This evidence concerns the gene CXCL5 and metabolic dysfunction-associated steatotic liver disease.