IL-1β partially sustains the aggressive phenotype of CAL62 cells via a novel mechanism mediated by Glo1 inhibition, which drives MG-H1 accumulation and, in turn, activates TGF-β1-mediated FAK signaling. Effects of Glo1 inhibition, under IL-1β administration, on (A) intracellular levels of MG-H1, evaluated by ELISA; (B) TGF-β1 and p-FAK levels, measured in the culture supernatant or lysate of CAL62 cells, respectively, by ELISA; and (C) migration and invasion capabilities, evaluated by specific assays. Histograms indicate mean ± SD of three different cultures each tested in triplicate. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to untreated cells.