Several elegant previous in vivo studies utilizing either CRISPR-based or gene knockout approaches demonstrated that loss of SETD2 promotes LUAD tumorigenesis in the canonical KRASG12D-driven LUAD mouse tumor model (Walter et al., 2017; Johnson et al., 2001; Jackson et al., 2001; Rogers et al., 2018; Xie et al., 2023). The gene discussed is SETD2; the disease is neoplasm.