Deletion of the insertion in breast cancer cells increased chromatin accessibility, leading to upregulation of LINC00636 and CD47, enhanced resistance to nutrient-deprivation-induced apoptosis (mediated by CD47), activation of senescence (driven by elevated LINC00636), delayed cell death, and reduced infiltration of CD80<sup>+</sup> pro-inflammatory macrophages, changes that represent tumor-promoting features. The gene discussed is CD80; the disease is breast cancer.