In addition, one study showed that cardiomyocyte inactivation of ANGPTL2 synthesis using AAV6-shAngptl2 injection following heart failure in mice reduced circulating levels of ANGPTL2 and improved cardiac function [68], and recent data suggest that ANGPTL2 secreted by HSC in the circulation may exert local roles in its microenvironment to maintain stemness [83], supporting indeed that cell-specific production of ANGPTL2 may be associated with specific organ defects/function. This evidence concerns the gene ANGPTL2 and heart failure.