The pathogenesis of HES is mediated by “piecemeal degranulation” or eosinophil activation and secretion of the granule cationic proteins (such as eosinophil peroxidase, eosinophil cationic protein, eosinophil-derived neurotoxin, and MBP1) and eosinophil-expressed cytokines (such as RANTES [regulated on activation, normal T expressed and secreted] and interleukin [4, 9]). Here, RNASE2 is linked to hypereosinophilic syndrome.