We previously reported that the treatment of cardiomyocytes with doxorubicin (Dox), an anti-cancer drug, promotes complex formation of TRPC3 protein, a major component of receptor-activated cation channels, with Nox2 [20,21], and extracellular ATP released from neonatal rat cardiomyocytes (NRCMs) evoked by stresses such as Dox and nutrient deficiency induces formation of TRPC3-Nox2 protein complex via P2Y2 receptor stimulation and resultant ROS production in NRCMs [24]. Here, CYBB is linked to cancer.