Previous studies demonstrate that CD147 overexpression correlates with aggressive clinicopathological features and poor prognosis in GC patients [24], primarily through its ability to upregulate matrix metalloproteinases MMP-2/MMP-9 [25], activate pro-angiogenic pathways via VEGF receptor cross-talk [26], and drive epithelial–mesenchymal transition through STAT3/AKT/ERK signaling [27–29]. Here, AKT1 is linked to gastric cancer.