Moreover, myocardial hypoxia activates fructose metabolism in human and murine models of cardiac hypertrophy through HIF-1α-driven activation of splice factor 3b subunit 1 (Sf3b1) and SF3B1-mediated splice switching of KHK-A to KHK-C (Mirtschink et al., 2015). The gene discussed is SF3B1; the disease is cardiac hypertrophy.