AKT1 and neoplasm: Notably, clusters 1 and 3 exhibited greater enrichment in oncogenic signaling pathways or targets, such as TNFA signaling, PI3K/AKT/MTOR signaling, and TGFβ signaling; pro-tumor signaling pathways, such as Epithelial-mesenchymal transition signaling; proliferation pathways, including G2M signaling, E2F signaling, MTORC1 signaling, and MYC signaling, offering a plausible rationale for clusters 1 and 3 displaying a lower survival rate and a pro-tumor microenvironment (Figure 3B).