KRAS and acute lymphoblastic leukemia: Accordingly, KRASG12D mutant Reh B-ALL cells showed reduced intracellular and extracellular levels of methionine and accumulation of MTA in the culture medium compared with wildtype cells, due to KRAS-mediated activation of the AKT/mechanistic target of rapamycin kinase (mTOR) signalling that induced methionine catabolism through AMD1.