Specifically, activation of NOX4 signalling secondary to inhibition of PLAC8 expression resulted in marked upregulation of signal transducer and activator of transcription 3 (STAT3), transcription factor Jun (c-Jun), and cellular tumour antigen p53 as candidate downstream promotors of redox-sensitive CB-ECFC VEGF-dependent angiogenic functions in this setting. The gene discussed is JUN; the disease is neoplasm.