Notably, patients in clusters 1 and 2 exhibited enhanced responses to ICIs, with cluster 1 demonstrating a poorer survival rate compared to cluster 2, likely due to the tumor microenvironment favoring pro-tumor immunity involving TNFA, PI3K/AKT/MTOR, and TGFβ signaling pathways (28, 29). The gene discussed is MTOR; the disease is neoplasm.