KIN17 is a DNA and RNA binding protein involved in DNA replication and damage response pathways. The protein functions as a bridge between DNA replication and repair machinery through high molecular weight complexes 1. KIN17 binds double-stranded DNA with preferential affinity for curved DNA structures and binds RNA through its C-terminal domain, supporting multiple aspects of genome maintenance including mRNA processing and splicing. Mechanistically, KIN17 recruits the R-loop regulator DHX9 to R-loop sites, enabling efficient DNA damage clearance and promoting cell survival 1. In esophageal squamous cell carcinoma, elevated KIN17 expression facilitates cancer progression by suppressing tumor-intrinsic innate immunity through R-loop resolution. Depletion of KIN17 accumulates R-loops, activating the STING pathway via NFκB signaling and triggering innate immune responses 1. This positions KIN17 as a critical regulator that coordinates DNA damage responses with immune surveillance, representing a potential therapeutic target for enhancing immunotherapy efficacy in cancers where DDR-mediated immune suppression occurs. KIN17's role in resolving noncanonical STING activation identifies it as a novel nexus between genome stability and anti-tumor immunity.