SEMA3A and fatty liver disease: As we did not delete Sema3a selectively in LSECs (because no LSEC-specific Cre mouse line was used), we also consider the possibility that other types of ECs contribute to the positive outcome of the EC-specific deletion of Sema3a; however, hydrodynamic injections performed by Zhou et al. to selectively silence or overexpress Nrp1 (coding for the co-receptor for SEMA3A) in the liver of DIO mice recently revealed that less NRP1 leads to reduced hepatic steatosis, whereas more NRP1 leads to increased hepatic steatosis62.