Encouragingly, adrenal-specific targeting opportunities may exist: tumor-suppressive roles of FOS [43,44] and JNK-phosphorylated JUN [45], alongside evidence of MAPK pathway hyperactivity in functional adenomas [[35], [36], [37]], suggest that pharmacological inhibition of JNK/ERK signaling (e.g., via small-molecule inhibitors) could provide a means to selectively normalize AP-1 activity in diseased tissue, potentially reversing hormone excess. The gene discussed is JUN; the disease is adenoma.