<unk> s arise from the nonmyelinating-type Schwann cells and can occur anywhere in the body. Gene involved in the pathogenesis of plexiform<unk>  is NF1 which codes for<unk> n that leads to loss of RAS control causing increased activity of downstream RAS pathways involved in increased cell growth and survival. Plexiform<unk>  may be caused by the bi-allelic inactivation of the<unk> tosis type I tumor suppressor gene. On gross pathology, a nonencapsulated superficial mass is the characteristic finding of localised or diffuse<unk> ; whereas the "bag of worms" appearance is the characteristic finding of plexiform<unk> . On microscopic histopathological analysis, nerve fibers, schwann cells, spindle cells with wavy nuclei without pleomorphism, shredded carrot collagen, moderate increase of cellularity vis-a-vis normal dermis, blood vessels, mast cells, pseudomeissnerian bodies, and varying degrees of myxoid degeneration are characteristic findings of<unk> . However, plexiform<unk>  shows a characteristic target sign on histopathology, representing a central core of collagenous and fibrillary tissue with peripheral less densely cellular myxoid tissue. Electron microscopy of<unk> s shows Schwann cells enclosing axons in plasmalemmal invaginations (mesaxons).
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