These observations prompt us to speculate that Pbsn+/Spink1− LEs (Gata2/3-specific LE1/LE-AP, LE2/LE-ADP, and LE7/LE-VPPbsn or Spdef-specific LE8/LE-LP) may be the cell-of-origin for most PRostatic ADenocarcinoma (PRAD), whereas the Spink1+/Pbsn− LEs (Bhlha15-specific LE-VPSpink1) may have a higher predilection to drive SPOP mutant PCa, where human SPINK1 is elevated (52). This evidence concerns the gene SPOP and posterior cortical atrophy.