Dooley et al. identified NFIB amplification/overexpression within murine tissue of mice genetically engineered by TRP53 and RB1 conditional deletion, showing that NFIB expression was essential for proliferation and viability during transformation of murine SCLC and reported also recurrent NFIB amplification in about 15% of primary human SCLC [271]. This evidence concerns the gene NFIB and small cell lung carcinoma.