Background: beta-catenin gene mutations have been reported in vast majority of pilomatrixomas (PMXs). P-catenin, a component of the adhesion molecules of the cytoskeleton, is degraded at the cytoplasm. Excess cytoplasmic beta-catenin enters into the nucleus and activates the transcription of several genes encoding c-myc, cyclin D1 and others. Sublocation of beta-catenin has been demonstrated by immunohistochemistry. The aim of this study was to determine the role of P-catenin-related proteins in various benign trichogenic tumors.