We thank Cunningham et al. [1] and Ruscitti et al. [2] for their commentary on our article [3] on the Macrophage activation syndrome (MAS)-like lung pathology in COVID-19 pneumonia. In order to clarify the classification of MAS, we proposed two types of MAS that fit along the immunological disease continuum of inflammation against self; modified for loss or gain of function [4]. It may turn out that some of the hyper inflammation related features of COVID-19 are due to overzealous killing of virally infected cells by CD8+ cytotoxic T-cells and COVID-19 related antigen driven expansion of CD4+ helper T-cells with increased pro-inflammatory cytokine production. Such a scenario would be analogous to the gain of function that occurs in adaptive immunity with chimeric antigen receptor (CAR)-T cells where the induced MAS can be treated with anti-IL-6R [3]. This pattern of inflammation occurs in immunocompetent subjects and is also known as secondary haemophagocytic lymphohistiocytosis (sHLH). To what degree this exists for COVID-19 infection awaits elucidation.