STING1 and neoplasm: An increase in the immunological infiltrate in the tumor microenvironment can be promoted through the release of damage-associated molecular patterns (DAMPs) by immunogenic cell death, chemokine secretion, and the immunostimulatory effect of the type-I interferon (IFN-1) pathway mediated by the cyclic GMP-AMP (cGAMP) synthase (cGAS) and its downstream adaptor stimulator of interferon genes (STING) [17,18,19].