PRKD3 and neoplasm: These disparate observations lead us to speculate whether in TNBC PKD2 and PKD3 are indeed interdependent for dimer formation and activity, as previously shown in HeLa cells (Bossard et al., 2007), or whether, instead, abnormal expression of PKD3 alone is sufficient to increase its activity through the formation of homodimers, thereby promoting tumor progression.