Triple negative breast cancer (TNBC) is an aggressive subtype of breast cancer, which currently has a paucity of targeted treatments. PEAK1 and NRBP1 are pseudokinases implicated in human cancers, their TNBC-related functions and mechanisms were explored during my PhD. I identified that CAMK2, an interactor of PEAK1, is required for PEAK1-promoted TNBC development. Pharmacological inhibition of CAMK2 blocks oncogenic roles of PEAK1. My findings support the notion that PEAK1 in combination with CAMK2 could be used as companion biomarkers to select patients for anti-CAMK2 treatment. My work also established pro-tumorigenic functions of NRBP1 in TNBC, highlighting NRBP1 as a candidate molecular target, and its regulating signalling pathways could be developed into therapeutic options.