In this regards, it was suggested that antagonism of the P2Y14 receptor could prevent the progression of COVID-19-induced systemic inflammation, which often leads to severe illness and death cases, as well as that P2Y14 receptor inhibition by its selective antagonist PPTN could limit neutrophil recruitment and NETosis, hence, limiting excessive formation of oxygen reactive species and proteolytic activation of the kallikrein–kinin system and subsequent bradykinin storm in the alveolar septa of COVID-19 patients [35]. The gene discussed is KLK4; the disease is COVID-19.