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We shown that, in distinction to classical opioid receptors, ACKR3 isn't going to trigger classical G protein signaling and isn't modulated through the classical prescription or analgesic opioids, such as morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists such as naloxone. Instead, we proven that LIH383, an ACKR3-selective