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The fact that we did not observe such a group by task interaction may be due to the extent of the lesions of the frontopolar group, which included, but were not restricted to, the frontopolar region.
As with ARG80, this interaction may be due to a transcriptional function of Pif1.
Thus, despite the low p values, the observed interaction may be due to chance.
Lack of interaction may be due to the small sample size of two of the smoking categories and also to the limited number of follow-up measurements.
The absence of a clear main effect or interaction may be due, in part, to substantial variability in context similarity effects during delayed recollection.
These conflicting results for the 5-HTTLPR × stress interaction may be due to differences in sample age, ethnicity (e.g., 5-HTTLPR allele frequency varies considerably according to ethnic background), as well as the methods used to rate predictors and outcomes.
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The many significant interactions may be due to the small sample size at high L. humile densities.
The interactions may be due to different patient populations or variable standard of care.
Nevertheless, we cannot exclude the possibility that the observed interactions may be due to linkage disequilibrium (LD).
These CPT-specific interactions may be due to the fact that CPT generates DNA TopI adducts and Tel1 is hyperactivated by DNA ends that are covalently bound to proteins, such as the Top1 DNA adduct (Fukunaga et al. 2011).
All the above-described functional interactions may be due to different factors, including the sharing of co-receptors, and receptor interactions, but they might also be due to complex interactions between S100A8/A9 proteins and other molecules, like those occurring between S100A4 and amphiregulin [ 58] or S100B and basic fibroblast growth factor [ 59, 60].
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