If one assumes nevi and phacomatoses to have been determined by deviated ontogenesis either at the, level of embryonal somatic cells or at the genetical level, the clinico-histological phenomena actually we encounter may be well explained. In case of nevocytic (melanocytic) nevi, deviatedly determined undifferentiated cells in the embryonal neural crest, by the effect of erroneous DNA-code(s) bestowed on them, are assumed to differenciate toward the cell spectrum spanned between the melanocyte and Schwann cell and to migrate to the skin to constitute the nevus tissue. When thus assumed, various features of the nevus tissue are clearly understood. For instance, the nevus cells which appear to have originated from the epidermis or nerves are actually the nevus cells having migrated with epidermal melanocytes or Schwann cells to grow on the foothold of the epidermis or the nerves. Similar explanation is possible for blue nevi and cellular blue nevi. If an adequate germ tissue is selected for other sorts of nevi, the origination of the latter from the former is possible to be explained. The mélanose neurocutanée of Touraine or Melanophakomatose of Musger, a phacomatosis simplest in its pathogenesis, differs from the nevocytic nevus only in the point that its phacomatoblast(s) (cf. nevoblast[s] of Pinkus-Mishima) with insufficient differentiating ability affected by their erroneous DNA-code(s) are distributed not only to the skin but also to the central nerve organs. The phacomatoblast(s) in v. Recklinghausen phacomatosis may be assumed to originate from the neural crest. The way of its (their) differentiation is bifurcated toward melanocyte on one hand and Schwann cell on the other. However, phaeochromocytoma reported to occur frequently in this phacomatosis, suggests the multiplicity of the differentiation of its phacomatoblast(s). The phacomatobiast(s) of Bourneville-Pringle phocomatosis may be assumed to originate from the embryonal mesenchyma. It (they) differentiates toward various directions, to be distributed to the skin, kidney, and other organs according to its fate, and to constitute abnormal tissue, i. e. the Bourneville-Pringle tissue. The Bourneville-Pringle tissue is the essential constituent in its each lesion and makes complex with other abnormal constituent(s) induced by it. If the explanation analogical to that of skin and kidney lesions is valid for the brain, its lesion (tuberous sclerosis) is likely to be induced by the Bourneville-Pringle tissue, though the evidence of this concept is not yet established. The pathogenesis of many other phacomatoses is possible to be explained by similar ways though there are still phakomatoses whose pathogeneses are not yet explained, i. e. Peutz-Jeghers syndrome, Gorlin-Goltz syndrome, et al.