AKT1 and Miyoshi myopathy: TAK-242 and TLR4 siRNA treatment in MM cells not only reduced HMGB1 and TLR4 expression (Figure S3) but also significantly downregulated multiple key molecules, including MyD88, NF-κB, ERK, AKT, Ki67, Cyclin D1, MMP2/9, and MT1-MMP These results suggest that the HMGB1-TLR4 signaling axis regulates essential pathways involved in MM cell proliferation, invasion, and survival.