These encompassed four predicted cancer driver mutations that were acquired during transformation of non‐malignant MCF10A cells to malignant DCIS.com cells (HRAS, EPHA7, MAP3K12, and PCSK5), and three that were acquired during transformation of MCF10DCIS.com cells to invasive cells (MCF10Ca1a and MCF10Ca1h) (PTPRD, TP53, and VSP13A) (Figure 1E; supplementary material, Figures S1 and S2). Here, PTPRD is linked to ductal breast carcinoma in situ.