Because Lyn (i) is an upstream non-receptor tyrosine-protein kinase within the BCR signaling and other receptor signaling pathways, it is (ii) highly expressed in CLL and bystander cells of the B-CLL TME (15, 31), and (iii) inhibition of Lyn downstream kinases BTK and PI3K reduces the EV release, we speculated that Lyn might also influence the tumor-supportive EV communication of stromal cells, both by raising the EV release (quantity) and influencing the EV composition (quality). Here, LYN is linked to neoplasm.