Considering that STING expression can be stimulated by the accumulation of cytosolic DAMPs, which are often found in cancer cells with a high degree of genomic instability (summarized in [34]), it could be hypothesized that cancer entities with a lesser degree of genomic instability such as prostatic adenocarcinomas [35], renal cell carcinomas [36], or neuroendocrine neoplasm [37] may be less prone to STING expression than cancers with high levels of genomic alterations such as SQCCs [38] or pulmonary [39] and pancreatic adenocarcinomas [40]. This evidence concerns the gene STING1 and renal cell carcinoma.