Our experimental observations demonstrate that SOS1 disruption specifically produces very significant therapeutic benefits, not only by markedly blocking development of the LUAD tumor cells but also by impairing the pro-tumorigenic effect of the surrounding stromal cells in the TME, thus supporting the consideration of SOS1 as a bona fide, actionable therapy target for developments of drugs/therapies against LUAD. The gene discussed is SOS1; the disease is neoplasm.