We identified 8 distinctive mutations (ASXL1, DNMT3A, GNBI, JAK2, PPM1D, SF3B1, SRSF2, TET2) and categorized the presence of any CH mutation as ALL.[15] The most common mutations of CH are DNMT3A, TET2, and AXSL1, which are epigenetic regulators, followed by PPM1D involved in DNA damage repair, JAK2 and GNB1 involved in cellular signaling, and the less common SF3B1 and SRSF2 mutations with roles in alternative splicing.[30] The exact role of these mutations in the pathogenesis of CH and related physiological impact is not fully elucidated. This evidence concerns the gene GNB1 and cyclic hematopoiesis.