Additionally, nonsense mutations in the Apelin Receptor (APLNR), which interacts with JAK1 to strengthen the IFN-γ response, were detected in patients with advanced melanoma or lung cancer resistant to ICBT; restoration of APLNR improved survival of mice with APLNR-defective melanomas treated with ICBT by increasing the responsiveness of tumour blood vessels to IFN-γ and augmenting the effectiveness of anti-tumour T cells [51]. Here, JAK1 is linked to neoplasm.