Aberrant PRC2 activity produces gene repressive epigenetic marks in multiple 
diseases and led to identification of Ezh2 as a drug target. Recent studies have 
shown that the epigenetic reader protein EED, associated with Ezh2 in PRC2, has 
an additional function to stimulate the PRC2 activity after binding to H3K27me3. 
Optimizing a compound known to block the H3K27me3 site in EED discovered by 
in-house screening, Novartis scientists have now produced a compound that shows 
durable tumor regression in a lymphoma xenograft model.