Activation of naive CD8⁺ T cells with antigen in the absence of skewing cytokines triggers their differentiation into effector CTL, which induces death of target cells. We show that CD8⁺ T cells activated in the presence of the cytokines IL‐6 or IL‐21 plus TGF‐β similar to CD4⁺ T cells, develop into IL‐17‐producing (Tc17) cells. These cells display greatly suppressed cytotoxic function along with low levels of the CTL markers: T‐box transcription factor Eomesodermin, granzyme B and IFN‐γ. Instead, these cells express hallmark molecules of Th17 program including retinoic acid receptor‐related orphan receptor (ROR)γt, RORα, IL‐21 and IL‐23R. The expression of the type 17 master regulator RORγt is causally linked to Tc17 generation, because its overexpression stimulates production of IL‐17 in the presence of IL‐6 or IL‐21. Both, upregulation of the type 17 program as well as suppression of CTL differentiation are STAT3 dependent. Furthermore, Tc17 cells producing IL‐17 but not granzyme B are also detectable in EAE, a mouse model for multiple sclerosis. Our data point to the existence of mutually exclusive CTL and Tc17 developmental pathways in vitro and in vivo.