Given the propensity for tumors to develop resistance to CPIs through mechanisms potentially associated with upregulation of CD38 in tumor cells, which inhibit CD8-positive T-cell function via adenosine receptor signaling (8), and that modakafusp alfa binds with high specificity to a unique epitope of CD38 (13, 14, 20), there is a strong rationale to evaluate modakafusp alfa in combination with pembrolizumab. Here, CD38 is linked to neoplasm.