There are several proposed inflammatory stimuli, including glycosylated native collagen in the breast parenchyma [7], deposition of glycosylated end products that act as neoantigens [6, 11], underlying autoimmune disease [1, 12], antibody cross-reactivity to exogenous insulin [13] or insulin contaminants [14], and altered tissue degradation due to locoregional cytokine imbalances [6, 7]. Here, INS is linked to autoimmune disease.