This is supported by the finding that the physiological ligand of CRABP1, atRA, can be used to protect against isoproterenol-induced cardiomyopathy in wild-type mice but not in CKO mice, and suggests a therapeutic potential of atRA in specifically targeting CRABP1 to reduce CaMKII over-activation related pathologies [13]. The gene discussed is CAMK2G; the disease is cardiomyopathy.