Due to an intense dispute with a reviewer of one of our manuscripts on the issue whether our frequency of p53 immunostaining in prostate cancer was lower than the 50% suggested by another group due to protocol issues (in our opinion) or to missed heterogeneity in a tissue microarray (TMA) setting (the reviewer’s opinion), we were forced to experimentally demonstrate that the range of p53 positive prostate cancers could be brought from 2.5% to 98% solely by protocol modifications [7]. The gene discussed is TP53; the disease is prostate cancer.