BCL2L11 and dystocia: The fact that Trp53YC/YC females shared phenotypic traits with both Bim+/-Trp53-/- mice (neural tube defects) and FasL-/-Trp53-/- mice (dystocia) may seem relevant, because Bim and FasL are both regulators of apoptosis and autophagy that also regulate immune responses (Sionov et al., 2015; Taylor and Ng, 2018).