Pungency is not taste, but pain. Accordingly, it was thought that isolation of a capsaicin receptor would lead to the development of novel antipungent and antinociceptive agents. After fierce world-wide competition, a gene for capsaicin receptor TRPV1 was isolated by Dr. David Julius at the University of California at San Francisco in 1997. Dr. David Julius was awarded the 2021 Nobel Prize in Physiology and Medicine for his discovery of the receptor for temperature (TRPV1 and TRPM8). TRPV1 was found to be activated not only by capsaicin, but also heat stimulus over 43 degree C, which is known to cause pain in humans and monkeys. Therefore, TRPV1 is a molecule activated by multiple nociceptive stimuli, indicating that TRPV1 can explain polymodal nociceptive neurons. It was also found that mice lacking TRPV1 don't feel pungency or pain upon exposure to capsaicin or noxious heat stimulus, indicating that TRPV1 works as a pain sensor at an in vivo level. Despite extensive efforts, no chemical targeting TRPV1 has become available in the market for controlling pain. The structure of TRPV1 at an atomic level was clarified with Cryo-EM by the David Julius and Yifan Cheng group in 2013. However, It has not yet been clarified how heat stimulus opens TRPV1. We need more research to develop antipungent or antinociceptive agents targeting TRPV1 in the future.