The biological importance of these LN‐LN interactions is exemplified by a group of human disorders where missense mutations affecting the LN domains of the LAMA2, LAMB2 or LAMA5 genes give rise to syndromic disorders; muscular dystrophy in merosin‐deficient muscular dystrophy for LAMA2, kidney and ocular developmental defects in Pierson syndrome for LAMB2, or defects in kidney, craniofacial and limb development for LAMA5.18, 19, 20, 21, 22, 23. This evidence concerns the gene LAMB2 and Pierson syndrome.