The observed effect of SFU-use on HbA1c can be explained by: (1) SFUs directly inhibit activity or growth of one or more of the WBF-011 formulation strains, (2) SFUs impact host glycemic control (e.g. constitutive enhancement of insulin secretion) in a way that abrogates the effect observed among the no-SFU participants randomized to WBF-011, (3) SFU usage correlates with a clinical stage of T2D that is more advanced, limiting capacity for improvement during the study. The gene discussed is INS; the disease is type 2 diabetes mellitus.