PRKCD (protein kinase C delta) is a calcium-independent, diacylglycerol-dependent serine/threonine kinase with dual and context-dependent roles in cell fate determination. In response to DNA damage, PRKCD promotes apoptosis by activating pro-apoptotic transcription factors like BCLAF1 and p53, and by phosphorylating mitochondrial regulators BAX and BAK 1. Conversely, in cancer cells, PRKCD promotes survival through NF-κB and AKT1 pathway activation, inducing chemoresistance 2. PRKCD phosphorylates Y313 to activate Src and p38 MAPK signaling, particularly in triple-negative breast cancer progression 3. Beyond apoptosis regulation, PRKCD functions in immune tolerance—PRKCD deficiency causes monogenic lupus and autoimmune lymphoproliferative syndrome 45. PRKCD also regulates PRKN-independent mitophagy through ULK1/ATG13 recruitment 6 and mediates antifungal immunity via CARD9 phosphorylation 7. In COPD, PRKCD promotes inflammatory responses, apoptosis, and mucin hypersecretion 8. In radiotherapy contexts, PRKCD expression increases post-radiation and correlates with improved survival and immune infiltration in lung cancer, suggesting miR-26b-5p-PRKCD axis modulation of radiosensitivity 9. These findings position PRKCD as a pleiotropic regulator of immunity, cell death, and cancer progression with therapeutic potential.