How warmth is detected is not fully understood at the molecular level. Here, the authors identified neuronal subpopulations in dorsal root ganglion (DRG) and sympathetic neuron cultures that responded to non-painful heat but not to agonists of transient receptor potential (TRP) ion channels that are implicated in thermosensation. In cell lines that share properties with sympathetic neurons, they determined that TRPM2 could mediate such responses. Knocking out Trpm2 in mice decreased the proportion of warmth-sensitive DRG neurons, and such mice had deficits in sensing warm temperatures, indicating that TRPM2 is needed for detecting non-painful heat.