MYC and hepatocellular carcinoma: In our previous work, we demonstrated that the co‐occurrence of MYC, TP53R249S and KRASG12D is sufficient to transform PHHs into in situ HCC, with all of them being indispensable for this process.[7] However, the concurrent presence of all these three genetic alterations in a single HCC case is infrequent, which presents significant challenges in translating our findings regarding their interactions into clinical applications.