There were 118 subjects with gene expression **data** passing quality control from CD4+ lymphocytes in Asthma BRIDGE who reported taking inhaled corticosteroids as a controller medication in the previous year. These subjects had mean Chronic Asthma Control Scores (CACS) of 10.8 (+/− 6.9), shown in Fig. 1 In Asthma BRIDGE, the SMARCD1 gene (SWI/SNFrelated matrix-associated actin-dependent regulator of chromatin subfamily D member 1) strongly interacted with age to indicate higher CACS on inhaled corticosteroids, with a doubling of expression associated with an (Fig. 2). In the replication population, GALA II, the age-by-SMARCD1 interaction was associated with poorlycontrolled asthma compared to subjects with controlled asthma, with a ratio of odds ratios relative to control of 1.72 (95% CI [1.42, 2.10], p = 3.8 × 10 − 8 ), indicating increasing probability of being in the poorly-controlled group with age. We observed that both the specific study within Asthma BRIDGE and self-identified race were strongly  (Table 1): GRAAD and CAG are adult studies and CARE is a study of children. Similarly, CARE is predominantly non-Hispanic white with a minority population of Hispanic white; while GRAAD and CAG are mostly African American. Since we wanted to focus on the interaction between gene expression and age in asthma control, we did not include either of these demographic variables in our main analysis. However, there was no significant association of race or study with SMARCD1 expression after adjustment for age (ANOVA, p = 0.29 and p = 0.3, respectively).