The role of HMGB1 in modulating the Akt/mTOR pathway to foster therapy-induced protective autophagy is a conserved mechanism, as evidenced in synovial sarcoma, where HMGB1-mediated suppression of Akt/mTOR signaling was identified as the key mechanism decreasing sensitivity to oxymatrine, further validating this axis as a central target for intervention across diverse malignancies [100] (Figure 2). The gene discussed is AKT1; the disease is synovial sarcoma.