Considering that most PIN lesions derived from PTEN‐transgenic mice will progress to tumour, in contrast to PIN lesions derived from the p53‐transgenic models 35, the high levels of SLC16A3 only in PIN lesions from PTEN models corroborates once more the involvement of MCT4 in disease progression. This evidence concerns the gene PTEN and prostate intraepithelial neoplasia.