Notably, however, the size of tumour developed in mice injected with p53−/− cells expressing 2KR mutant is smaller than that in mice p53−/− cells transfected with an empty vector (Mock) under doxorubicin-treated conditions, indicating that 2KR is still capable of suppressing tumour development by inducing p53 phosphorylation and BAX expression, although much less efficiently than wild-type p53. Here, BAX is linked to neoplasm.