ORMDL3 and asthma: Reduced IL-2 production and fate skewing, as noted in human T cells homozygous for 17q12–21 asthma risk SNPs and elevated ORMDL3 expression, may result from reductions in sphingolipid generation that hinder the shift to anabolic metabolism and macromolecule biosynthesis required during clonal T cell expansion and Th1 effector differentiation (49).