We will not discuss in depth the known relationships between FOS, Lamin A/C and prostate cancer. We leave this discussion for later, as Lamin A/C will also appear in our study of the other prostate cancer dataset studied in this paper. Lamin A/C appears as a member of a set of genes with reduced expression for higher grade primary prostate cancer samples (note that the current analysis that gave FOS as a biomarker is on lymph node metastatic samples like here). However, we would like to point out a connection that is currently hypothesized between Lamin A/C and FOS, the gene we have just discussed. Ivorra et al. have recently proposed that ''lamin A overexpression causes growth arrest, and ectopic c-Fos partially overcomes lamin A/C-induced cell cycle alterations. We propose lamin A/C-mediated c-Fos sequestration at the nuclear envelope as a novel mechanism of transcriptional and cell cycle control'' [74] . In addition: ''c-Fos accumulation within the extraction-resistant nuclear fraction (ERNF) and its interaction with lamin A are reduced and enhanced by gain-of and lossof ERK1/2 activity, respectively.'' [75] . These novel interactions between LMNA and FOS, their putative role in prostate cancer metastasis and their seemingly different behaviours in prostate cancer lymph node metastases warrant further investigation.