PON1 and brain neoplasm: Previous studies have shown that the Notch suppressor complex PON/Numb is preferentially localized to progeny cells (Suzuki et al., 2006; van Oers et al., 1999) and that ectopic activation of Notch generates a brain tumor phenotype attributable to excess NBs, suggesting that Notch activity is required for NB self-renewal (Wang et al., 2006).