The activation of the ERK pathway serve as a stimulus for HSCs to exit the self‐renewal program and transition into the differentiation phase.[50] CREBBP activity in bone marrow stromal cells influences the microenvironment that supports HSCs, that loss of CREBBP in murine haematopoietic stem and progenitor cells (HSPCs) leads to increased development of B‐cell lymphomas.[51] Previous studies have shown that CREB is a classical target of PI3K/AKT signaling.[52] In our study, adding exosomes to embryonic stem cells significantly upregulated PI3K and AKT phosphorylation (Figure 5E). This evidence concerns the gene AKT1 and B-cell non-Hodgkin lymphoma.