MTAP and neoplasm: Interesting highlights in this space include a functional association of Werner syndrome ATP‐dependent helicase dependency and microsatellite instability (MSI),[41, 46] loss of enzyme methylthioadenosine phosphorylase (MTAP) in cancer cells and enhanced sensitivity to the inhibition of epigenetic regulator protein arginine methyltransferase 5 (PRMT5)[47, 48] and more recently, the therapeutic potential of stimulating NOTCH signaling in cancers driven by inactivation of this critical tumor suppressor.[49]