The identification of IL-6 as the main pro-inflammatory factor responsible for inducing the overexpression of tumour-related RAC1B raised the question of whether IL-6 was also involved in the higher RAC1B expression levels that we observed in non-polarized Caco-2 cells in Figure 1C. As shown in Supplementary Figure S4A, the RAC1B protein levels in non-polarized Caco-2 cells did not change after addition of neutralizing anti-IL-6 antibodies, nor did they correlate with increased STAT3 phosphorylation levels. Here, IL6 is linked to neoplasm.