Our results are in accordance with the results of Eksioglu‐Demiralp who showed that HGF has a survival‐protective effect on B‐CLL cells in vitro.28 Thus, we hypothesize that lower levels of SPINT2/HAI‐2 induced an increase in HGF secretion, which acts on de novo AML cells through a paracrine loop, stimulating the HGF‐MET pathway and resulting in an improved adhesion of CD34+ de novo AML cells to HS‐5 stromal cells and CD34+ cell survival, which is an important mechanism of leukaemia chemotherapy resistance. The gene discussed is HGF; the disease is B-cell chronic lymphocytic leukemia.