In contrast, other driver gene mutations, such as JAK1/2 and AT-rich interactive domain-containing protein 1A (ARID1A) mutations, were reported to be associated with T-cell infiltration and favorable response to ICI treatment with high expression of tumor antigens as well as co-occurring KRAS mutations and TP53 inactivation [21,90]. This evidence concerns the gene ARID1A and neoplasm.