In addition, this study demonstrated that selective ORMDL3 expression in ASM regulates likely novel pathways not studied in universal ORMDL3-Tg mice, including ORMDL3 regulation of ASM hypertrophy, TPM proteins involved in ASM hyperplasia, increased expression of ASM contractile genes (Serca2b and Sm22), increased Orai1 Ca2+ channels, and increased intracellular Ca2+ levels, providing additional pathways through which ORMDL3 may regulate ASM contractility, which may contribute to the development of AHR in childhood onset asthma, which is highly linked to ORMDL3 on chromosome 17q12-21. The gene discussed is ORMDL3; the disease is childhood onset asthma.