COVID‐19 and SSc share similar physiopathological alterations, such as diffuse microvasculopathy and neofibrogenesis [2]; in this regard, SARS‐CoV‐2 infects both endothelial cells and macrophages causing diffuse endotheliitis with thrombotic manifestations, as well as a specific lung CD163+ macrophage polarisation driving excessive fibroproliferation [1]. This evidence concerns the gene CD163 and systemic sclerosis.