The most cited molecular hypothesis for the pathogenesis of PPCM is a prolactin (PRL)-mediated mechanism postulated by Hilfiker-Kleiner et al. 2 3 Their work with rat models of PPCM showed abnormal upregulation of PRL cleaving factors (such as Cathepsin-D) compared with wild types.2 4 This increased expression of cleaving enzymes leads to the production of the angiostatic and proapoptotic 16 kDa isoform of PRL, which induced HF in the rats via the induction of the micro RNA-146a. This evidence concerns the gene PRL and hydrops fetalis.