Furthermore, long-term treatment of C2C12 myoblasts and C2C12 differentiated myotubes with IR exosomes were observed to imitate cancer cachexia, such as elevation of MuRF1 and MAFbx/Atrogin-1 expression and decrease in p-mTOR and p-AKT in a fashion similar to the siRNA exosome-treated group as compared with GBM exosome-treated groups (Figure 4D, Figure S3B). The gene discussed is AKT1; the disease is glioblastoma.