Moreover, in KitV558Δ/+ GIST mice, Liu et al. reported that imatinib reduced the expression of MHC-I molecules by inhibiting type I IFNs production and signaling, attenuated tumor immunogenicity, decreased the infiltration of CD8+ T cells, and thus weakening the antitumor immune responses [195], which may partially explain the limited efficacy of immunotherapy for GIST patients having received prior imatinib therapy. Here, CD8A is linked to neoplasm.