Given that blocking GRPR by pharmacological or genetic approaches has been identified to alleviate prolonged pruritus via ablating spinal phosphorylation of ERK in mice with squaric acid dibutylester-induced contact dermatitis [30], it will be of great interest to determine whether IFN-I restricts ERK activation via the modulation of GRPR on spinal itch-responsive neurons in our itch models. The gene discussed is GRPR; the disease is contact dermatitis.