Likewise, we find CNVs explain a large share of variation for genes in specific cancer types that have previously been linked to CNVs, like KRAS in both LUSC (31% added variance explained) [71–73] and LUAD (33% added variance explained), MDM2 in LGG (31% added variance explained) [74], DROSHA in BLCA (28% added variance explained) [75], FGFR2 in STAD (26% added variance explained) [76–78], and EGFR in LGG (25% added variance explained) [79, 80]. This evidence concerns the gene KRAS and cancer.