Sciarretta et al. (2015) showed that cardiac-specific mTORC2 disruption through rictor deletion in 6-month-old mice resulted in Mst1 activation, leading to dilation and impaired cardiac function. Increased cardiac fibrosis and apoptosis were also observed in rictor knockout mice, where they developed severe heart failure in response to pressure overload. In addition, compensatory hypertrophic response was also attenuated, suggesting that Rictor/mTORC2 regulates pressure overload-induced cardiac hypertrophy (Sciarretta et al., 2015). Here, RICTOR is linked to heart failure.