LATS2 and diabetes mellitus: While we could show by multiple experimental settings that LATS-induced effects on β-cell apoptosis and autophagy is mediated by mTORC1 activation, it is equally possible that LATS2 activation and mTORC1 hyperactivation act in parallel under stress- and diabetogenic conditions to dysregulate the β-cell compensatory machinery and induce β-cell death, dysfunction and thus metabolic failure and diabetes.