Technological advances in methods for purification, expansion and universal or tumor-specific activation of patient-derived T-cells could pave the way towards the elimination of MYC-driven tumors through local production of IFN-γ by CD4+ T-helper cells, which potentially would have the dual effect of upregulation of p27 expression in tumor cells together with increased immunosurveillance. This evidence concerns the gene CDKN1B and neoplasm.