Furthermore, the inflammatory response not only did not decrease but increased in MyD88 deficient mice, accompanied by the increase in cardiac expression of TLR4 and TRIF, indicating that MyD88-dependent signaling functions as a negative regulator of pro-inflammatory pathological response mediated by TRIF in the context of high dose Ang II-induced cardiac hypertrophy (97), and infusion doses of Ang II may cause MyD88-dependent signaling functions in cardiac hypertrophy differing from the usual response. Here, MYD88 is linked to cardiac hypertrophy.