The noncovalently tethered dimers of MSA-2 could bind STING with nanomolar affinity, and the acidic tumor microenvironment would substantially increase the cell entry and retention of MSA-2 and its dimerized interaction with STING, thus leading to a superior antitumor potency of combined MSA-2 and anti-PD-1 treatments. This evidence concerns the gene STING1 and neoplasm.