We have demonstrated that rosiglitazone (which can exert its effects via activation of the nuclear transcription factor PPARγ and/or via PPARγ-independent mechanisms) can target multiple pathways implicated in the pathogenesis of CM including inflammation, oxidative stress, and endothelial activation, and is capable of initiating or enhancing neuroprotective mechanisms including the induction of neurotrophic factors. Here, PPARG is linked to cutaneous mastocytosis.