PCA of 242 pretreatment biopsies revealed a major homogenous cluster with a few deviations and no obvious associations with pCR or HER2 heterogeneity status, nor with other clinicopathologic features including tumor cellularity and lymph node and hormone receptor status (Figure 1B and Supplemental Figure 3A), suggesting that T-DM1+P resistance might be driven by specific pathways rather than global transcriptomic differences. The gene discussed is ERBB2; the disease is neoplasm.