HRAS and hyperplasia: However, oncogene mutations have emerged recently as potential drivers in several benign salivary gland entities including BRAFV600E mutations in sialdenoma papilliferum [33], AKT1 mutations in intraductal papilloma/ papillary mucinous neoplasms [33, 34], PIK3CA mutations in sclerosing polycystic adenoma [35–37], IDH2 mutations in striated duct adenoma [38], and HRAS/CTNNB1 mutations in a subset of intercalated duct hyperplasia/adenoma [39].