Regarding the frequency of tumor formation, we observed an overall low penetrance and latency in the murine tumors derived from heterozygous Sox2-cre::Smarcb1fl/+ (penetrance of 18%) and inducible Sox2-creERT2::Smarcb1fl/fl (penetrance of 22%) mouse models lacking Smarcb1 expression in comparison to tumors derived from the ubiquitous Rosa26-creERT2::Smarcb1fl/fl (penetrance of 40%). The gene discussed is SOX2; the disease is neoplasm.