Renalase-dependent cell signaling may also be debated in the context of COVID-19, since the triggering of renalase receptor, PMCA4b [18, 25], in vitro, results in a rapid increase of phosphorylated ERK1/2, p38, and PI3K/Akt, while downregulating c-Jun N-terminal kinases (JNK) [18, 25, 69, 70]. The gene discussed is RNLS; the disease is COVID-19.