Furthermore, rats with loss of function KCNK3 mutations develop the characteristic hyperproliferative cell phenotype seen in PAH and manifest pathologic activation of kinases like SRC and extracellular signal-regulated kinase (ERK) 1/2, as well as the normoxic activation of HIF-1α (Lambert et al., 2019). The gene discussed is HIF1A; the disease is pulmonary arterial hypertension.