Interrogation of the tyrosine phosphorylation patterns characteristic of the other p53-null subgroups revealed that phosphorylation of the atypical kinase Peak1/SgK269 [55] was elevated in tumour 14845 and to a lesser extent the subgroup containing 3049, 1202 and 1201, whereas phosphorylation of Prex2 characterised tumours 14845 and 3049, where it was accompanied by enhanced phosphorylation of Pik3r2 (Figure 7). This evidence concerns the gene PEAK1 and neoplasm.