Fluid shear stress activates PI3-K/AKT, ERK1/2, and p38 pathways in human chondrosarcoma cells via a cAMP- and IL-1β-dependent mechanism, as evidenced by the inhibition of AKT, ERK1/2 and p38 phosphorylation by a cAMP inhibitor and an anti-IL-1β neutralizing antibody. Here, AKT1 is linked to chondrosarcoma.