In the cardiac variant of Fabry’s disease, patients have some alpha-galactosidase A activity and present later in life, often with only cardiac manifestations, although proteinuria can also be present.7 The cardiac variant, first described in 1990,25,26 may be due to alternative splicing in the alpha-galactosidase A gene,27 and in the first published case series, five of seven patients had no mutations in the coding regions despite very low levels of mRNA.7 The aetiology of the cardio-tropism of the cardiac variant of Fabry’s has not been elucidated. This evidence concerns the gene GLA and Fabry disease.