In addition, CD73 also exerted its functions in a enzymetic-independent way, which was suggested by the phenomenon that enzymetic activity blocked by APCP treatment does not completely reverse the effect of CD73 overexpression (Gao et al., 2017) Previous studies have shown that CD73 was positively with abnormal EGFR and PI3K/AKT signaling, which is the factors and hallmarks of tumor progression (Zhi et al., 2012; Ma et al., 2019). The gene discussed is AKT1; the disease is neoplasm.