The adapter protein GRB2 is central to T-cell receptor (TCR) signal transduction, yet its precise role in setting activation thresholds remains controversial. To clarify its functions, we generated stable GRB2-knockout (KO) Jurkat T-cell lines using CRISPR/Cas9 gene editing. Systematic analysis of TCR/CD3-stimulated GRB2-KO cells revealed widespread signaling hyper-activation: proximal ZAP-70 phosphorylation was drastically increased, and downstream signaling was markedly enhanced, evidenced by elevated ERK and PLC-γ1 phosphorylation along with heightened intracellular Ca²⁺ influx. In contrast, LAT phosphorylation was significantly decreased in GRB2-KO cells, indicating that GRB2 acts downstream or in parallel to constrain activation even when LAT phosphorylation is blunted. Intriguingly, loss of GRB2 was accompanied by reduced THEMIS protein expression, suggesting a potential link between GRB2 and THEMIS levels in human T cells. These findings support a role for GRB2 as an important negative gatekeeper of TCR signaling whose absence promotes hyperactivation despite reduced LAT phosphorylation, while to enhanced activation pathways while highlighting an intriguing association between GRB2 and THEMIS. Together, our results provide new mechanistic insights into the regulatory constraints governing human T-cell activation.