Here, differences in the pattern of TSG inactivation between C-TL and G-TL are likely due to a cascading effect from the differential probability of perhaps one keystone event (e.g. increased physical chance of Bcl11b loss by interstitial deletion/recombination) which due to the co-operative/redundant nature of the pathways means that each successive mutation/lesion defines the selective pressure for the next event(s) driving tumours towards phenotypes reflecting one or more oncogenic networks. Here, BCL11B is linked to neoplasm.