The cylindromatous gene Cyld encodes a deubiquitylase (DUB), which regulates NF-jB activation. CYLD deficiency results in faulty innate and adaptive immune systems in mice, the basis for which remains incompletely understood. In this issue of The EMBO Journal, Sun and colleagues report that CYLD-deficient mice develop the innatelike lymphocyte called natural killer T (NKT) cells but lose them to death, which resulted from overactivation of NF-jB and low interleukin-7 receptor (IL-7R) expression. Consequently, CYLD-deficient NKT cells poorly respond to IL-7 and do not upregulate inducible costimulatory (ICOS) receptor, molecules that serve as survival signals in other cellular contexts. These findings integrate disparate prior knowledge revealing the molecular basis for NKT cell homeostasis and have implications for understanding why human NKT cell frequency varies between individuals.