NKG2D-dependent killing of non-virally infected hepatocytes in hepatitis A exacerbates liver damage (Kim et al., 2018) and may also play a role in inflammatory lung disease (Borchers et al., 2009), and there is evidence that NKG2D ligands are expressed in the lungs in COVID-19 (Wauters et al., 2021), so it could be that a late and persistent expansion of bystander-activated effector T cells in severe COVID-19 could be a driver of lung pathology. Here, KLRK1 is linked to hepatitis A virus infection.