LEPR and myelofibrosis: Since LepR+ BMSCs have been identified as key components of hematopoietic microenvironment52,60,61 and responsible for myelofibrosis,62,63 it was reasonable that enhancement of TFEB-mediated autophagy by CXM102 treatment in LepR+ BMSCs could reduce the myelofibrosis, but further studies are needed to illustrate the detailed mechanisms.