Utilizing transgenic technology, it has been discovered that mice lacking either TREK1 or TREK2 channels exhibit notable hypersensitivity to both thermal and mechanical stimuli.[23, 24] Furthermore, research conducted on animal models of pain has shown the crucial role of TREK1 and TREK2 channels in modulating nociceptive hypersensitivity in various conditions such as migraine, spinal nerve ligation (SNL)‐induced neuropathic pain, formalin‐induced inflammatory pain, prostatitis pain, and oxaliplatin‐induced pain. Here, KCNK2 is linked to prostatitis.