MYD88 and fibrosis: While the molecular mechanism of anthracycline-induced cardiac fibrosis and inflammation is still unclear, mounting evidence suggests a pivotal role of nucleotide-binding domain-like receptor protein-3 (NLRP3) inflammasome and myeloid differentiation primary response protein (MyD88) myddosome in the development of cardiac inflammation and fibrosis induced by anthracycline administered either alone or in combination with immune therapy, such as immune checkpoint inhibitors [33, 34].