Scientists now have a better understanding of why sensory neurons sometimes register light touches as painful (a common and debilitating condition called mechanical allodynia) following injury in mice and humans, thanks to the results of two studies. They identified an ion channel involved in sensory neuron signaling as an underlying culprit for the development of hypersensitivity to pain, a finding that could lead to new therapeutic strategies for allodynia. Humans and other mammals contain distinct subsets of sensory neurons that can distinguish between sensations such as the brush of a feather and the prick of a thorn. However, inflammation, nerve injury and other forms of trauma can scramble these sensations, causing innocuous touches to become intensely painful. This condition is a major concern for researchers and clinicians working in the clinical pain space, but further investigation is needed to determine the contributors that distort pain perception at the molecular level. Swetha Murthy and colleagues zeroed in on the function of the Piezo2 ion channel, which has previously been shown to play a key role in touch sensation. After finding that activating Piezo2-expressing neurons induced pain sensations in mice, the researchers discovered that rodents deficient in Piezo2 did not register pain in response to soft touches in several models of mechanical allodynia. In a second study, Marcin Szczot and colleagues used imaging techniques to study sensory neurons in mice and saw that Piezo2 was necessary for responses to gentle mechanical stimuli (including air puffs and vibration) but not normal pain sensation. They also identified four individuals with mutations resulting in loss of Piezo2 function and saw they did not perceive light brushes as painful when applied to an inflamed spot on the forearm, indicating blocking Piezo2 function could potentially prevent allodynia without affecting normal pain responses.