The distinction between the two scenarios—whether Arid1a loss cooperates with oncogenic Ras to induce PDAC formation (as proposed [3,4,5,6]), or invasive cancers arise via an “escape” phenomenon in the setting of growth constrained precursors–goes beyond semantics, given the occurrence of ARID1A mutations across a multitude of epithelial pre-cancers [45]. Here, ARID1A is linked to cancer.