IKBKG and incontinentia pigmenti: Thus, it is hypothetically possible that cutaneous manifestations in IP originate from IKBKG mutation, whereas extracutaneous anomalies in IP patients originate from some gene mutation other than IKBKG. According to this hypothesis there is an option that combinations of mutations of IKBKG and some other gene(s) are responsible for final IP phenotype expression – skin changes and associated extracutaneous anomalies.