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Another group of scientists found an additional pathway in which the T-2 toxin generates pro-apoptotic conditions in the cellular milieu by initiating a cascade reaction involving Fas up-regulation on chondrocyte surfaces, followed by the up-regulation of p53 proteins which in turn increases the Bax/Bcl-2 and Bax/Bcl-xL ratios, simultaneously activating the caspase-3-dependent apoptotic pathway [74]