In this connection, because of their augmented chromosomal instability and correlation with LUAD patient survival, lung cancers harboring MEN1 inactivation may be dependent on a fast Pol II elongation rate to generate R-loops, abundantly accumulating DSBs, thereby supporting tumor growth, which to some extent explains the selective lethality of lung cancer cells to splicing inhibitors. This evidence concerns the gene MEN1 and lung carcinoma.