STAT3 may enhance resistance to conventional chemo- and radio-therapies by inducing the expression of survival proteins and cell cycle genes, which are well-known STAT3 targets (as Bcl-2, survivin, c-myc, cyclin-D1, and Mcl-1), and by down-regulating tumor-suppressor genes either directly, like p53, or indirectly via ZEB1 induction (85–92). The gene discussed is BCL2; the disease is neoplasm.