Ours is, however, the first report of CD36 expression being increased in human HF in the absence of diabetes mellitus, or analysed in terms of ICM or DCM, but our results, taken together with the data for PPARA, PGC1A and HFABP and previous reports of increased FA levels perturbing mitochondrial function [24], [26]–[28] could make sense in one or more ways. This evidence concerns the gene PPARGC1A and hydrops fetalis.