Targeted sequencing of T-ALL patient samples has also demonstrated the frequent co-occurrence of PRC2 component mutations with NOTCH1-activating mutations.66 The same study also suggested that silencing of the PRC2 components EZH2 and SUZ12 upregulates typical NOTCH1 target genes including HES1 and DTX1 and results in decreased apoptosis in the presence of a γ-secretase inhibitor that inhibits NOTCH1 signalling.66 This suggests that the loss of PRC2 potentiates NOTCH1 protein signalling and increases NOTCH1 target gene expression, despite inhibition of NOTCH1. The gene discussed is NOTCH1; the disease is acute lymphoblastic leukemia.