Furthermore, the interaction of DCAF12 with the TRiC/CCT complex enables quality control over key oncogenic effectors, including STAT3 and mTOR components (Raptor and mLST8),[22, 23] activating the STAT3 and mTOR pathways, which are essential for cellular proliferation, migration, and stemness.[59, 60] While our study focused on cytoskeletal and YAP/STAT3/mTOR pathways, previous studies have implicated DCAF12 in TGF‐β signaling in other cancers.[39] Given the role in metastasis,[61] this conserved regulatory mechanism may further augment the pro‐metastatic function of DCAF12 in lung cancer. The gene discussed is MTOR; the disease is cancer.