SOAT1 and COVID-19: Overall, the Janus kinase (JAK)/signal transducer and the activator of the transcription (STAT) pathway were at the centre of attention for driving hyperinflammation in COVID-19, i.e., the SARS-CoV-2 infection triggers hyperinflammation through the JAK/STAT pathway, resulting in the recruitment of dendritic cells, macrophages, and natural killer (NK) cells, as well as differentiation of B cells and T cells progressing towards cytokine storm [6] (Figure 1).