Genomic sequencing revealed a prevalence of mutations in TP53 (53.3%) and PTEN (40.7%) in mCRPCs [208], suggesting an important interaction between these two tumor suppressors in suppressing the acquisition of a PCSC-like stage and/or the induction of the lineage plasticity of PCSCs during the progression of metastasis and CRPC. The gene discussed is PTEN; the disease is neoplasm.