Cancer with homologous recombination deficiency (HRD), particularly ovarian cancer, preserves basal genomic stability by alternative DNA damage repair (DDR) mechanisms, making HRD cancer cells susceptible to DNA damage therapies such as poly (ADP-ribose) polymerase inhibitors (PARPi).1-3 A mass of aberrant endogenous DNA fragments produced by HRD tumors can activate innate immunity by the cGAS-STING pathway, etc.4 Collectively, HRD is a potential biomarker for DNA damage therapy and immunotherapy. Here, STING1 is linked to hypoparathyroidism-retardation-dysmorphism syndrome.