ATM and thalassemia: Exploratory analysis in that study hinted those co-mutations in DNA damage repair genes (i.e., ATM, Ataxia-Telangiectasia Mutated; ATRX/DAXX, Alpha Thalassemia/Mental Retardation Syndrome X-linked/Death-Domain-Associated Protein pathway) were associated with improved outcomes on KRAS G12C inhibitors [58]—possibly because they confer a more genomically unstable phenotype that is more sensitive to therapy.