Skin-resident CD8 ⁺ T cells include distinct interferon-γ–producing [tissue-resident memory T type 1 (T _RM 1)] and interleukin-17 (IL-17)–producing (T _RM 17) subsets that differentially contribute to immune responses. However, whether these populations use common mechanisms to establish tissue residence is unknown. In this work, we show that T _RM 1 and T _RM 17 cells navigate divergent trajectories to acquire tissue residency in the skin. T _RM 1 cells depend on a T-bet–Hobit–IL-15 axis, whereas T _RM 17 cells develop independently of these factors. Instead, c-Maf commands a tissue-resident program in T _RM 17 cells parallel to that induced by Hobit in T _RM 1 cells, with an ICOS–c-Maf–IL-7 axis pivotal to T _RM 17 cell commitment. Accordingly, by targeting this pathway, skin T _RM 17 cells can be ablated without compromising their T _RM 1 counterparts. Thus, skin-resident T cells rely on distinct molecular circuitries, which can be exploited to strategically modulate local immunity.