Importantly, our long-term analyses until 12 months of age (when most diseased animals had to be euthanized according to ethical regulations for animal experimentation) demonstrated in particular that the LUAD tumor burden was always significantly reduced in SOS1KO/KRASG12D mice in comparison to SOS2KO/KRASG12D mice for the whole duration of the life of these animals (Fig. 1h, i), clearly indicating a preferential functional contribution of SOS1 over SOS2 with regards to both the early stages of initiation and the later stages of progression of KRASG12D-driven LUAD in mice. The gene discussed is SOS1; the disease is neoplasm.