SNAI1 and glioma: In gliomas, SMC4 drives two critical oncogenic programs: (1) cell proliferation and cell cycle progression: SMC4 overexpression accelerates G1/S transition in vitro and enhances tumor growth in xenograft models (Figures 3C–J; Figure 4), consistent with its role in chromosomal condensation during mitosis (12); (2) metastatic spread via TGF-β/Smad Signaling: SMC4 promotes glioma cell migration and invasion by upregulating EMT markers (N-cadherin, SNAI1, ZEB1) and activating phosphorylated Smad2/3 (Figure 2H).