Domain-specific mutations in both genes were also subtype- and ER/PgR-specific, whereby all tumor subtypes related to ER/PgR positivity were significantly more frequently mutated in the TP53 DNA binding domain than in the TAD and oligomerization domains; subtypes related to ER/PgR absence more frequently had more mutations in the helical than in the transactivation domain of the PIK3CA gene. The gene discussed is PGR; the disease is neoplasm.