Since the synthesis of the cholesterol upstream metabolite IPP promotes immuno-killing, but low levels of cholesterol trigger chemoresistance, we tried to disrupt this metabolic balance by setting up a pharmacological strategy that increases IPP without varying cholesterol levels, with the goal of achieving a chemo-immuno-sensitization of NSCLC tumors with low levels of TFEB. Here, TFEB is linked to non-small cell lung carcinoma.