CD1a autoreactive T cells activated by lipid presentation are overrepresented in human skin lesions associated with atopic dermatitis and psoriasis, and the component of C42, doubly unsaturated sphingomyelin (42:2 SM) may function as an inhibitory agent by obstructing the possible binding of TCRs presented on CD1a self‐reactive T cells.[119] During stable physiological conditions, the preferential loading of “blocker” lipids into CD1a disrupts TCR recognition. This evidence concerns the gene CD1A and atopic eczema.