The dynamics of different SMAD2/3-BAF complexes could provide the necessary stem cell–like developmentally plastic or “metastable” capacity of CSCs, as we have previously shown in human embryonic stem cells for mixed lineage leukemia/COMPASS.24 Because BAF subunits ARID1A and BAF180/Polybromo are mutated in a subset of PDACs, it suggests possibly divergent mechanisms of how the BAF complexes could promote CSC characteristics in PDACs. The gene discussed is SMAD2; the disease is leukemia.