Our interpretation of these data is that SARS-CoV-2 infection triggers the underneath genetic susceptibility due to RTEL1 variants, leading to both a need for higher respiratory support in the acute phase, as well as to a chronic fibrotic process, which may eventually result in open ILD depending on specific (often private) variant (see Additional file 1: Table S1). The gene discussed is RTEL1; the disease is interstitial lung disease.