Instead, PI3K/AKT/mTOR signaling emerged as a downregulated signaling pathway upon menin inhibition, revealing a different mechanism behind HCC cell proliferation (Figure 3).21 Additionally, we found more sites that gained accessibility following menin inhibition, suggesting that disrupting menin-MLL1 leads to a novel transcriptional response. The gene discussed is MTOR; the disease is hepatocellular carcinoma.