The observation that the increase in SRSF2 protein level induced massive procaspase-3 cleavage when associated with gefitinib in H358 cells, which express wild-type and non amplified EGFR protein, may be particularly relevant for patients with lung adenocarcinomas without EGFR mutations, as one of the challenges is to understand why only some of them respond to EGFR tyrosine kinase inhibitors. The gene discussed is SRSF2; the disease is lung adenocarcinoma.