In lung cancer, KLF5 mediates cell stemness promoted by α-Catulin; [46] in hepatocellular carcinoma, KLF5 overexpression enriches cancer stem cell-like populations, enhancing drug resistance; [47] in triple-negative breast cancer, metformin inhibits stemness in these cells by targeting KLF5 for degradation; [48] inflammatory cytokine TNF-α can partially promote basal-like breast cancer (BLBC) cell stemness through the activation of the KLF5-EphA2 axis; [49] and in colon cancer, miR-4711-5p suppresses tumor cell stemness by downregulating KLF5 expression through direct binding [50]. Here, EPHA2 is linked to neoplasm.