“…The authors indicated that the HCM group presents more significant structural and functional cardiac changes, resulting in more pronounced symptoms and the need for drug interventions. 7 These findings corroborate the pathophysiological mechanism implicated in the origin of both diseases, while in HCM mutations in cardiac sarcomere genes trigger hypertrophy, disarray, and fibrosis, in FD, the deposition of Gb3 in cardiomyocytes activate inflammatory and neurohormonal mechanisms involved in the formation of hypertrophy and tissue fibrosis, although indirectly and to a lesser extent. 8 The decrease in the glomerular filtration rate was more significant in FD since renal impairment occurs progressively and early; however, it is important to highlight that in this context of diagnosis differential, it is a finding that must be carefully considered.…”