JUN and neoplasm: The oncogenic mechanism of CAMSAP2 mainly involves several classical signaling pathways: in hepatocellular carcinoma, inhibition of HDAC6 through the JNK/c-Jun pathway promotes microtubule acetylation-mediated tumor metastasis [7]; in colorectal cancer, activation of the JNK/c-jun/MMP-1 signaling axis drives cellular invasion [13]; and in gastric cancer, it promotes epithelial–mesenchymal transition (EMT) progression through upregulation of TGF-β signaling [56].