Considering that wild-type p53 has the ability to abrogate RUNX3 expression through inducing miR-34a [85], it is plausible that the gain-of-function mutation of Trp53R172H (codon 175 in humans), which recapitulates a germline mutation from Li–Fraumeni Syndrome [87], might not only enhance RUNX3 transcription but also convert the function of RUNX3 from tumor suppressive to dominant oncogenic. Here, TP53 is linked to neoplasm.