In 1967, Seligman and Maier proposed the famous theory of learned helplessness based on animal experiments. They theorized that animals learned that outcomes were independent of their responses—that nothing they did mattered—and that this learning undermined trying to escape. In 2016, at the time when the theory was put forward for 50 years, Maier and Seligman reviewed the development of the theory, especially the biological mechanism of learned helplessness, and proposed their surprising rethinking: learned helplessness (passivity in response to shock) is not learned. It is a default, unlearned response to prolonged aversive events and mediated by the serotonergic activity of the dorsal raphe nucleus, which in turn inhibits escape. This passivity can be rescued by learning control, with the activation of the medial prefrontal cortex, which subserves the detection of control leading to the automatic inhibition of the dorsal raphe nucleus. So animals learn that they can control aversive events, but the passive failure to learn to escape is an unlearned reaction to prolonged aversive stimulation. For all researchers working in related fields, this rethinking is astonishing and worthy to be paid attention. Therefore, we briefly reviewed the origin and development of the theory of learned helplessness, and introduced the rethinking and the related neural mechanisms. Base on this review, we then discussed and commented on the rethinking. First of all, it is a good example for psychologists to test psychological theorization by using empirical data form neuroscience researches. Nevertheless, there are still some points in the rethinking need to be considered. First, there is still not sufficient evidence which Seligman and Maier employed in the rethinking to deny the existence of “learned” helpless. For example, it is truly evidenced that escapable shock but not exactly equal inescapable shock, increased the activation of projecting neurons in ventromedial prefrontal cortex (vmPFC), but it is still not clear whether vmPFC received the same amount of inputs under both escapable and inescapable shock conditions. Secondly, considering validity of the triadic experimental design, it is less proper to apply the original triadic design to laboratory rats in studies of learned helplessness, because laboratory rats unlikely have established expectation of control in their prior experience. Actually, the original design could not precisely reveal the psychological processes of learned helplessness, because expectation of subjects to control was not ensured. However, the expectation to control and loos of it induced by failure are the crucial ingredients for development of learned helplessness. Therefore, the neuroscience evidences with original design in rats could not strongly support the rethinking that learned helplessness is not learned. Finally, there is no doubt that learned helplessness exists in humans. When someone encounters prolonged aversive events which are uncontrollable, such as continuous failures in examinations, he/she will lose the expectation of success, give up trying, and even suffer from disorder like depression. Therefore, it is necessary to proceed to study learned helplessness, but a more appropriate experimental design is needed. In order to reveal the psychological processes and neural correlates of learned helplessness, we proposed a modified design based on the original triadic paradigm. One group of subjects was firstly exposed to a prolonged escapable stress treatment, which aims to establish the controllable expectation, and then to a prolonged inescapable treatment, accompanied with the yoked and na?ve groups. This modified design ensures the learning of controllability and then uncontrollability, while separates the effects of stressor per se by using the yoked and na?ve groups. The modified design highlights cognitive ingredient for learned helplessness, and thus have a better constructive validity for study of learned helplessness or learned depression in humans.