In addition, in vitro and in vivo (db/db mice) studies were undertaken to examine whether NGR1 acts through estrogen receptor (ER)α-dependent activation of the AKT pathway and inhibition of TGFβ signaling, providing the rationale for NGR1 being a therapeutic candidate that can attenuate the development of DCM. This evidence concerns the gene AKT1 and familial dilated cardiomyopathy.