MYC is recurrently altered across ILC and a common driver of tumor progression and recurrence in ER-positive breast cancers generally, however this may not be the case in LobSig high tumors.47,48 The signature captures a biology driven by the combination of multiple different genomic alterations (amplifications of 1q, 8p, 11q, 17q12; mutations in TP53, ERBB2/3; losses of 13q). Here, CCL27 is linked to neoplasm.