The decreased expression of hsa-mir-26a-5p in AML can cause high expression of peroxiredoxin III, thereby promptly clearing the reactive oxygen species within cells and protecting tumor cells from oxidative stress injury (38, 39); In another study, researchers found that enforced expression of hsa-mir-26a-5p in AML cells was able to inhibit cell cycle progression by downregulating cyclin E2 expression, potentiated the antiproliferative effects of 1,25-dihydroxyvitamin D (3) (VitD) and stimulated myeloid differentiation by targeting E2F7 (40). The gene discussed is CCNE2; the disease is neoplasm.