Importantly, we found very high levels of activated RET (phosphorylated at tyrosine 1062) in the tumors developed by lamin B1–haploinsufficient mice and inverse correlation of lamin B1 and RET expression in lung cancer patients, supporting the notion that RET activation may play a key role in lung cancer development and progression upon lamin B1 loss. This evidence concerns the gene LMNB1 and lung cancer.