SUMMARY. In dark skinned subjects, delayed or “secondary” pigmentation from ultra‐violet light may be the only clinical sign of sunburn. It results from necrobiosis limited to the outer Malpighian layer and hardly extends deeper than this even when the dose exceeds the maximum possible from a day's natural sunshine. Preceding erythema is not merely masked by the pigment, but is often virtually absent. On the background of this natural skin resistance, the hyperkeratotic pellagrous lesion is interpreted as a marked reaction to mild or repeated ultraviolet injury followed by retention and ultimate cracking of the abnormal layers so produced. These layers are formed below the normal stratum granulosum when the initial damage is severe, but lie above the new stratum granulosum which forms underneath as the cells keratinize.