Our findings suggest that in addition to impacting the interaction of GATA4 with TBX5, the G296S mutation can also alter PGC-1α/ERRγ/GATA4 cooperativity which could contribute to the human disease phenotypes including cardiomyopathy which occurs in ERR-deficient mice10,11. This evidence concerns the gene SLC7A1 and cardiomyopathy.