At a granular level, primary KP tumors can be categorized into those that have undergone cell state changes that promote malignant progression, marked by amplification of signaling downstream of KRASG12D through the MAPK pathway (6, 7) and a relatively rare subset of KP tumors that have progressed to become metastatically competent, which is identified by the lost expression of the lineage specifying transcription factor NKX2-1 and acquired expression of the nonhistone architectural transcription factor HMGA2 which is normally restricted to embryonic cell types (5, 8). This evidence concerns the gene HMGA2 and keratosis pilaris.