This suggestion corresponds to the results of our study showing that over-expression of the miR-106b∼25 cluster in NASH-derived HCC, especially miR-93-5p, is accompanied by substantial decrease in the levels of E2F1, PTEN, and CDKN1A proteins, direct targets of miR-93 [19, 42, 43]. Here, PTEN is linked to metabolic dysfunction-associated steatohepatitis.