More recently, experimental studies on human ACTH-secreting tumor cell cultures have shown that, after incubation with dexamethasone, SSTR2 expression significantly decreased, with SSTR5 expression remaining stable (7, 10), suggesting that chronic glucocorticoid exposure is able to downregulate SSTR2, but not SSTR5, expression, which could be consequentially considered as the real potential target for SSA treatment in CD (4, 7). Here, SSTR5 is linked to neoplasm.