This pathway is integral to T1D pathophysiology through multiple facets: the presence of core cysteine residues in islet autoantigens can affect autoantibody binding, reduced cysteine‐dependent antioxidative defenses contribute to β‐cell oxidative stress, and cysteinyl leukotriene signalling can modulate insulin secretion, thereby linking inflammatory mediators to metabolic function [47, 48, 49]. Here, INS is linked to type 1 diabetes mellitus.