SETD2 and neoplasm: Combined with a lentiviral vector that expresses Cre recombinase, along with the essential CRISPR components, Cas9 and an sgRNA to Setd2, we and others have shown that inactivation of Setd2 in KrasG12D-driven lung adenocarcinoma promotes cellular proliferation very early after tumor initiation; an effect that is widespread amongst all developing tumors13,14.