PRKCQ (protein kinase C theta) is a calcium-independent serine/threonine kinase localized to chromosome 10 that functions as a critical mediator of T-cell receptor (TCR) signaling and immune responses. In T cells, PRKCQ phosphorylates CARD11 to activate the canonical NF-κB pathway and regulates transcription factors including NF-κB, JUN, NFATC1, and NFATC2, driving IL-2 production and T-cell activation 1. PRKCQ plays essential roles in Th2 cell development and Th17 cell differentiation during inflammatory responses, while having minor involvement in Th1 responses 1. Beyond immune function, PRKCQ mediates phagocytosis by phosphorylating WIP during macrophage antibody-dependent cellular cytotoxicity, enabling tumor cell phagocytosis 2. The kinase also regulates platelet signaling and may suppress insulin signaling by phosphorylating IRS1. Dysregulation of PRKCQ associates with multiple autoimmune diseases, including Vogt-Koyanagi-Harada syndrome, as demonstrated by genetic polymorphism studies 1. In cancer, particularly triple-negative breast cancer, PRKCQ promotes cell survival and chemotherapy resistance through suppression of pro-apoptotic Bim; PRKCQ inhibition enhances chemosensitivity 3. PRKCQ expression is also linked to breast cancer proliferation and inflammation via NF-κB pathway activation 4, while PRKCQ-AS1 lncRNA regulates cancer metabolism and paclitaxel resistance 56.