These organoids capsulate the molecular diversity and clinical heterogeneity of PCa subtypes, including TMPRSS2-ERG fusion, ETS translocation, SPOP mutation, SPINK1 overexpression, FOXA1 and PIK3R1 mutation, CHD1 deletion, PTEN deletion, and AR expression, and retain the genomic characteristics of primary tumors. The gene discussed is CHD1; the disease is posterior cortical atrophy.