DAPK2 (death-associated protein kinase 2) functions as a tumor suppressor kinase that regulates multiple cellular processes including apoptosis, autophagy, and immune responses 1. The protein acts through diverse mechanisms, with one isoform capable of phosphorylating MYL9 and inducing membrane blebbing and autophagic cell death in a calmodulin-independent manner. DAPK2 plays a critical role in activating autophagy through interactions with AMPK, mTORC1, and p73, while also inducing apoptotic pathways via p73 family and JNK interactions 1. Recent studies reveal DAPK2's importance in mitochondrial metabolism and cancer progression, where dysfunction leads to Mic60 lactylation and mitochondrial cristae remodeling, promoting EGFR-TKI resistance and metastasis in lung cancer 2. Additionally, DAPK2 shows connections to immune regulation, as related family member DAPK1 activity is inhibited by fumarate accumulation in CD8+ T cells, affecting anti-tumor immunity 3. The kinase demonstrates tumor suppressor functions across various cancers including gastric, ovarian, and breast cancers, making it a potential therapeutic target 1. DAPK2's multifaceted roles in cell death pathways, metabolic regulation, and immune responses highlight its significance in cancer biology and therapeutic development.