We also report detection of genomic loss of ERBB2 exon 16 (Ex16Alt) due to either intragenic deletion (Ex16Del) or splicing mutations (Ex16Splice) as a very rare (0.04% prevalence pan-tumor) but recurrent (33, 34) mechanism of ERBB2 activation associated with resistance to targeted therapies in some cancers [e.g., osimertinib and other EGFR TKIs in NSCLC (35) and trastuzumab in GEC (36)]. Here, EGFR is linked to neoplasm.