These findings are in agreement with those published earlier demonstrating that miR-31, miR-155, and miR-564 are down-regulated in CML cells [31], creating a therapeutic window wherein the molecular or therapeutic (as in our case using Ova) enhancement of miR-155 expression and/or activity could play a critical role in reversing the oncogenic effect of the activated Stat5 and the PI3K/AKT/mTOR signaling pathway. The gene discussed is PIK3CA; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.