This apparent contradiction arises from the context-dependent role of KCNIP3 expression in glioma: In fact, as shown in Figure 5D, KCNIP3 expression is higher in Cluster A. In the poor-prognosis Cluster B, KCNIP3 is relatively low but may be moderately upregulated as a compensatory response to counteract excessive pro-tumorigenic signaling. Here, KCNIP3 is linked to glioma.