We elected to investigate the genetic interaction of Nf2, Trp53, and KrasG12D further, by generating gRNAs to specifically target and disrupt the Nf2 and Trp53 loci (or a nontargeting control, gRNAscrm), which were then coinjected hydrodynamically with our KRASG12D expressing construct to define whether loss of these tumor suppressors can specifically cooperate with KRASG12D to promote tumor initiation. The gene discussed is NF2; the disease is neoplasm.