Inflammatory pain is a debilitating condition and a severe health burden; physiologically, it is a complex phenomenon with multiple contributing mechanisms. A new study published in The EMBO Journal reports that tissue inflammation results in local depletion of cholesterol in nociceptive nerves, causing a loss of lipid raft localization of a sodium channel Nav1.9 and, ultimately, resulting in potentiation of its activity. The discovered effect contributes to the inflammatory overexcitability of peripheral nociceptive nerve terminals resulting in inflammatory hyperalgesia. Topical application of cholesterol‐containing gels was able to offset this inflammatory pain mechanism thereby opening a novel avenue for therapeutic intervention.