Consistent with lineage specific tumour suppressor thresholds, Tp53-/- SH2B3± mice developed B-ALL in a manner that was strictly dependent on loss of the wild type SH2B3 allele [44], while SH2B3± mice developed a milder form of the myeloproliferative disease seen in SH2B3 -/- mice [45]. This evidence concerns the gene TP53 and neoplasm.