Intriguingly, the identified mechanism included the ability to reactivate wild-type p53 expression from the non-mutant allele and ERK-mediated stabilization of the oncogenic protein c-Myc; the second previously published effect, which activates cell proliferation in cancer cells, is based on the inhibition of ERK phosphorylation and associated c-Myc expression potentially involving acetylation. The gene discussed is TP53; the disease is cancer.