Our studies provide the rationale to consider whether a Trypanosoma cruzi infection induced decrease in β1AR sialylation might facilitate β1AR N-terminal cleavage, enhance agonistic antibody-dependent activation of the cAMP/PKA pathway (while dampening signaling via the cardioprotective ERK pathway), and promote adverse cardiac remodeling. The gene discussed is ADRB1; the disease is Chagas disease.