As for the biological function of ACHE in ccRCC, Figure 11(g) shows that a high level of ACHE could activate KRAS, interferon-γ and interferon-α, inflammatory IL6-JAK-STATS and IL2-STAT5 pathways in pan-cancer, especially in ccRCC, which indicated that ACHE was involved in immune regulation in cancer. This evidence concerns the gene ACHE and nonpapillary renal cell carcinoma.