Specifically, this approach, the inhibition of specific holoenzyme formation could be leveraged toward re-establishing balance in PP2A activity in patients that harbor the Aα-P179R or other PP2A Aα mutations that demonstrate marked loss of binding of tumor-suppressive B regulatory subunits (B56α and B55α) but had no effect on the association with Striatin family members. This evidence concerns the gene PPP2R5A and neoplasm.