Our GSEA analysis revealed that the high TEK expression group was enriched in pathways related to the “G2M checkpoint.” This is reinforced by established evidence that pharmacological inhibition of AKT/mTOR phosphorylation can induce G2/M phase arrest and apoptosis in cancer cells (Li et al., 2024), further supporting the notion that shikonin can regulate the balance between apoptosis and survival in renal cancer cells through the TEK-AKT/mTOR axis. Here, TEK is linked to renal carcinoma.