For example, in a mouse model of sterile fulminant hepatitis generated by tumor necrosis factor (TNF)-induced hepatocyte apoptosis, inducible genetic knockout of Ninj1 limited liver injury, demonstrating a role for NINJ1 in apoptosis-related plasma membrane rupture in vivo and highlighting the functional importance of NINJ1 in hepatitis pathogenesis (Kayagaki et al. 2023). Here, NINJ1 is linked to hepatitis A virus infection.