Thus, we speculate that carcinogenesis hinders a more extensive modulation of the transcriptional signature observed in the NAFLD model in the absence of Plin5. Finally, when comparing different pathways altered in NAFLD and NAFLD-related carcinogenesis, we identified several important effector molecules that have been previously reported in various models of NAFLD and HCC, including STAT3, p38, JNK, and Akt [44]. Here, STAT3 is linked to metabolic dysfunction-associated steatotic liver disease.