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Although we hypothesized that Ca^2+^ activity might lead to a SRE-driven pro-inflammatory response through activation of the SREBP-1 signaling pathway, we were not able to demonstrate this in our experiments. Inhibition of the NFκB pathway also did not decrease LPS-induced ApoE expression in Hepa 1–6 cells ([Figure 1](#ijms-21-00257-f001){ref-type=”fig”}). In addition, we also investigated whether Ca^2+^ activity might influence the SREBP-1 signaling pathway directly by using nuclear/cytoplasmic separation to investigate the subcellular localization of SREBP-1 and Ldlr in Hepa 1–6 cells. We found that SREBP-1 and Ldlr are found in both cytoplasm and nucleus in Hepa 1–6 cells and that LPS addition did not alter the subcellular localization of these two proteins. An explanation for the contrasting results regarding the effect of Ca^2+^ in the LPS/Aβ-induced inflammation is yet unclear and might be attributed to differences in the experimental protocols (different administration methods for Ca^2+^ as well as the different concentrations used) between our study and the previous studies. However, we aimed to provide a comparative study by using two different incubation methods (plate and bulk) and by using different concentrations of Aβ and Ca^2+^ and found that both had similar effects. We additionally found that cells stimulated with Aβ and Ca^2+^ together showed significantly greater
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