Tissue-resident memory T (Trm) cells are a recently defined population of memory T cells that persists at the site of previous infection and provide superior local immunity. Trm cells have been identified in almost every organ tested, including epithelial and solid organs. We sought to identify transcriptional regulators of Trm cell development by studying these cells in a number of different organs. Here we show that while Trm do share some commonalities, they also have distinct transcriptional requirements according to anatomic location. Our earlier data demonstrated that the two related transcription factors Hobit and Blimp1 enable tissue-residency in lymphocytes by preventing tissue egress. In the current study, we examined the individual contribution of several transcription factors to Trm cell development. A lack of Hobit alone caused defects in Trm cell development in all organs tested. Consistent with this, forced expression of Hobit enhanced Trm cell development. In contrast, T-bet was required for Trm cell development in some organs, but was dispensable in others. This differential transcription factor dependency was linked to distinct cytokine requirements for Trm cell development in different organs. Additionally, Trm cells that lack T-bet have an altered cytokine profile, including the induction of IL-17. Trm cell defects were enhanced in the absence of multiple transcription factors, suggesting functional redundancy and implicating a role for distinct transcriptional networks as drivers of Trm cell development in different organs. Together, these data demonstrate the adaptation of Trm cells to specific tissue microenvironments and highlight the importance of studying these cells in a variety of organs.