These observations prompts 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 (45). The gene discussed is SPOP; the disease is adenocarcinoma.