Moreover, SARS-CoV-2 infection via ACE2 can activate STAT3, which in turn can activate the so-called IL-6 amplifier [103], a mechanism for the hyperactivation of STAT3 that might trigger a positive feedback capable of self-amplifying the IL-6/STAT3 signaling in lung alveolar epithelial cells, thereby accelerating the transition from virus replication/spreading to COVID-19 clinical stages. Here, IL6 is linked to COVID-19.