The markedly increased levels of PCT in COVID-19 patients can be explained by several factors: a coexistent bacterial infection, prolonged invasive mechanical ventilation and the up-regulation of the signal transducer and activator of the transcription 3 (STAT3)-dependent pathway, which stimulates angiotensin-converting enzyme 2 (ACE2) and PCT production in monocytes [15,16,17]. The gene discussed is CALCA; the disease is COVID-19.