Mechanisms associated with this process include enhanced glycolysis in NSCLC cells to generate reductive metabolites which neutralize cisplatin-induced reactive oxygen species (ROS), inhibition of apoptosis by exosomal PKM2 via a PKM2-BCL2-dependent manner, and reprogramming of CAFs to produce an acidic microenvironment that promotes NSCLC cell proliferation and cisplatin resistance [93]. The gene discussed is PKM; the disease is non-small cell lung carcinoma.