These dynamics may explain the mixed and evolving immune landscapes observed in many tumours, which are shaped by their unique evolutionary genetic trajectory consisting of potentially co-occurring (or sequentially occurring) mechanisms favouring immune activation (e.g., via neoantigen production or cGAS-STING signalling activation) or immune suppression (e.g., via chronic inflammation, immunoediting, or activation of tolerogenic cytokine pathways such as IL-6/STAT3). The gene discussed is STING1; the disease is neoplasm.