At mucosal barriers, the T helper 17 (T_H17) cell population plays a fundamental role in controlling tissue homeostasis. The adaptability of this population to a more pro-inflammatory or anti-inflammatory function — that is, their functional plasticity and consequently heterogeneity — primarily depends on the environment. We would like to term this process environmental immune adaptation. Interfering with T_H17 cell adaptation leads to pathological consequences, including development of immune-mediated inflammatory diseases or even cancer. Several molecular mechanisms have been shown to participate in this process and recently, a better understanding of the transcriptional and metabolic profiling of T_H17 cells has shed light on a new level of complexity. Here, we offer a summary on the role of T_H17 cell plasticity in inflammatory diseases and cancer as well as the latest discoveries and controversies regarding the mechanisms that control the adaptability of the T_H17 cell population.