Combined, these observations suggest that cancer-derived point mutations in Aβ may lead to loss of tumor suppressive activity due to severely crippled catalytic function (as in the case of R233C) or as a result of skewed phosphatase activity against only a subset of substrates, as shown previously in the case of mutants like P65S that can bind the catalytic subunit, but not the tumor suppressive regulatory subunits B56α and B56γ. The gene discussed is PPP2R5A; the disease is neoplasm.