Th17 cells and their proinflammatory signature cytokine, IL-17, have recently replaced Th1 cells to be the essential Th effector population in autoimmune disease. This was based on a similar line of evidence that previously destined Th1 cells to be the sole encephalitogenic Th-cell effector type. However, as for the Th1-effector type before, an increasing amount of evidence is accumulating that questions the pivotal role of Th17 cells in autoimmunity. Recently, four high-impact articles were published that clearly show that Th1 and Th17 cells carry encephalitogenic properties, and dominance of either in an autoimmune setting can confer disease. In two mouse models for autoimmune neuroinflammation, it was suggested that Th1 and Th17 cells act in parallel, both exhibiting a different set of effector mechanisms.