We observed that the pathway terms selenocompound metabolism, cysteine and methionine metabolism, protein digestion and absorption, fat digestion and absorption were mostly enriched (Fig. 4b), implying an enrichment of pathways related to metabolic alterations, which is consistent with current knowledge about the tumor suppressor and the low-density lipoprotein (LDL) receptor functions of LRP1B [24]; the results suggested that the comutation of PIK3CA and HMCN1 could play a role in abrogating the oncogenic metabolic signature arising from LRP1B mutation. Here, PIK3CA is linked to neoplasm.