While previous studies suggested a link between dysadherin and CSC traits, showing that dysadherin overexpression enhances self-renewal and tumor-initiating potential, the underlying mechanisms remain unclear.14 Our results revealed that dysadherin activates the FAK/YAP/TEAD2 pathway to induce key pluripotency genes, thereby promoting CSC maintenance and therapy resistance. The gene discussed is TEAD2; the disease is neoplasm.