To quantify the ability of oncogenic BRAF and EGFR to initiate lung tumors and drive their expansion in vivo, as well as to uncover whether tumor suppressor effects are consistent across these oncogenic contexts in lung cancer, we initiated tumors with Lenti-D2G28-Pool/Cre in BrafCA-V600E;H11LSL-Cas9 (Braf;Cas9) and tetO-EGFRL858R;Rosa26LSL-rtTA3-ires-mKate/LSL-Cas9-2a-GFP (Egfr;Cas9) mice (Fig. 3A)36. Here, BRAF is linked to lung cancer.