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We shown that, in contrast to classical opioid receptors, ACKR3 will not set off classical G protein signaling and is not modulated because of the classical prescription or analgesic opioids, such as morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists for instance naloxone. As a substitute, we proven that LIH383, an ACKR3-se