Therefore, we suggest that cytoplasmic β-catenin accumulation subsequent to loss of functional NKX3.1 (Figure 6A) correlates with prostatic inflammatory atrophy, most likely facilitates the tumor heterogeneity (Figure 6B) and initiation that can be suppressed by androgen regulated NKX3.1 expression in prostate. This evidence concerns the gene NKX3-1 and neoplasm.