Our analysis of a publicly available dataset indicated that INHBA was upregulated in melanoma patients with progressive disease after anti-PD1 therapy.34 Furthermore, neutralization of endogenous Activin-A by a soluble form of ACVRIIB sensitized iBIP2 melanoma grafts to combined anti-PD1/anti-CTLA4 blockade, whereas INHBA gain-of-function in YUMM3.3 melanoma grafts inhibited the response. Here, CTLA4 is linked to melanoma.