We suspect the PIK3CA-PTEN combination is one such case: the PI3K pathway either harbours frequent activation events in the oncogenic PIK3CA kinase (96/156 breast tumours) resulting in accelerated cell growth and proliferation or reciprocally frequent inactivation events in the tumour suppressor PTEN (67/156) resulting in loss of negative-feedback to control cell proliferation; however we rarely see breast tumours harbouring both these events (8/156; p-value ≈ 0) possibly due to their detrimental effect on cancer cell survivability. Here, PTEN is linked to breast neoplasm.