Together these results are in agreement with Ferrarotto and colleagues9 and functionally reflect the good prognosis of p63-positive ACC type II and the poor-prognosis of myc-driven ACC type I. An increased level of UPR signaling observed in p63-negative ACCs marks the occurrence of ER stress in this tumor subgroup and provides further connection with myc oncogenic activation27. This evidence concerns the gene TP63 and neoplasm.