The aim of this study was to further investigate the molecular background of syndromic MEN1 parathyroid adenomas using fluorescence in situ hybridization, next-generation sequencing with copy number analysis based on the relative number of reads and allelic imbalances, and immunohistochemistry to determine the potential presence of hyperplasia or of multiple independent clones and the amount of Menin loss. This evidence concerns the gene MEN1 and parathyroid gland adenoma.