To corroborate this hypothesis, we tested whether the heterozygous loss of Pax5 (Pax5-het), a common second hit identified in murine and human B-ALL-associated ETV6-RUNX1 (Heltemes-Harris et al., 2011; Papaemmanuil et al., 2014; Martin-Lorenzo et al., 2018), would restrict the tumor cell type to B-ALL in Sca1-ETV6-RUNX1 mice, similarly to Kdm5c loss. This evidence concerns the gene RUNX1 and neoplasm.