In an effort to explore the mechanisms that transform NHPrE1/AR cells to form invasive cancers in vivo, we examined the expression of FOXA1, a well-established AR co-activator [29], as well as MYC and pSTAT3, two genes that are differentially recruited to the AR transcriptome [28], in tissue recombinants derived from NHPrE1/EV and NHPrE1/AR cells. This evidence concerns the gene AR and cancer.