In this communication, we show that distinct human RyR2 inherited mutations expressed in mammalian cells exhibit either unaltered or increased FKBP12.6 binding compared to wild-type. Oxidising conditions result in reduced FKBP12.6 binding, but to the same extent as for wild-type. Our findings suggest that FKBP12.6 regulation of RyR2 is unlikely to be the primary defect in inherited arrhythmogenic cardiac disease.