TIGIT and ductal breast carcinoma in situ: Clotting factors may directly facilitate destruction of the myoepithelial layer and progression to invasion or may create a “wound that does not heal.”8 The latter is supported the by coevolution of the immune microenvironment with breast cancer progression with for example, a reduction in activated CD8+ and TIGIT+ T cells and T‐cell receptor clonal diversity, but an increase in PD‐L1 expression with transition from DCIS to invasion.24