To achieve a more clinically relevant model, we integrated into the topology common co-mutations of KRAS found in over 1000 clinical lung adenocarcinoma patients [10], most frequently being P53 (about 40%) and LKB1/STK11 (about 20%), and KEAP1, to enable the efficient patient-specific translation of the model from bench to bedside (Figure 5A). This evidence concerns the gene STK11 and lung adenocarcinoma.