This study suggests that AKT could promote tumor differentiation in certain setting. PAX3-FKHR abolition in ARMS cells led to terminal differentiation, therefore, it is worth considering the potential role of AKT activation-dependent inactivation of PAX3-FKHR in this effort. Taken together, we venture that acute AKT activation should be evaluated for therapeutic benefit in ARMS and also in certain types of tumor.
Jothi, M., & Mal, A. K. (2012). Too much AKT turns PAX3-FKHR dead: A prospect of novel therapeutic strategy for alveolar rhabdomyosarcoma. Oncotarget, 3(10). https://doi.org/10.18632/oncotarget.713