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 neoplasm.