Until now, the only evidenced benefit for drug use in EMF-deterring progression of the inflammatory pathology, has revolved around steroids, with the list of trial drugs expanding to include, more lately, serotonin receptor inhibitors. Surgery, mainly that involving cardiomyoectomy of pathological lesions, has a role despite its infrequent use due to poor state of heart surgery available in regions where EMF is similarly prevalent. Ideally, all EMF patients with stage III and IV heart failure would benefit from a heart transplant. The foregoing picture underlines the need to devise novel, cheap and yet still effective medical interventions against EMF. In the past, the pathophysiology of EMF has been closely related to that of several other cardiomyopathies, including the hypereosinophilic syndrome, and Chaga��s disease. Specifically, all 23-Acetyl-alisol-C diseases are known to possess a spectrum of pathology that encompasses hypereosinophilia, fibrosis and or, in long standing cases, calcification. Recent studies have established molecular mimicry as the mechanisms for pathology in some of the above EMF related cardiomyopathies. Specifically, auto antibodies to the CG acidic C- termini of two Trypanosoma cruzi ribosomal proteins have been associated with the chronic cardiac pathology of Chaga��s disease in humans. Martin et al. have recently described, using 3dimensional modeling and docking experiments, a more clear interaction of the structural elements involved in the autoimmune mechanism of anti-P auto-antibodies cross-reaction and stimulation of the b1-adrenoreceptor, results that may lead eventually to the development of treatments to abolish receptor mediated symptoms in Chaga��s disease. Given the prior observed related pathology in both diseases, we hypothesized, that molecular mimicry may explain the pathology seen in both diseases too. By so doing, we also subhypothesized that the molecular insult in Chaga��s disease may bear similarity to the insult responsible for EMF.This study was conducted to examine the specific-hypothesis that resemblance between the Ctermini of the two T. cruzi ribosomal proteins TcP0/TcP2b and prior suspected causative insults for EMF explains the commonality of gross pathology.