Ovarian folliculogenesis corresponds to the development of follicles leading to either ovulation or degeneration, this latter process being called atresia. Even if atresia involves apoptosis, its mechanism is not well-understood. The objective of this project was to analyse global gene expression in pig granulosa cells of ovarian follicles during atresia. The transcriptome analysis was performed using 9216 cDNAs microarray to identify gene networks and candidate genes involved in pig ovarian follicular atresia. One thousand six hundred and eighty four significantly regulated genes were differentially regulated between small healthy follicles and small atretic follicles. Among them, two hundred and eighty seven genes had a fold-change higher than 2 between the two follicle groups. Eleven genes (DKK3, GADD45A, CAMTA2, CCDC80, DAPK2, ECSIT, MSMB, NUPR1, RUNX2, SAMD4A, and ZNF628) having a fold-change higher than 5 between groups could likely serve as markers of follicular atresia. Moreover, automatic confrontation of deregulated genes with literature data enlightened 93 genes as regulatory candidates of pig granulosa cell atresia. Among these genes known to be inhibitors of apoptosis, stimulators of apoptosis or tumor suppressors INHBB, HNF4, CLU, different interleukins (IL5, IL24), TNF-associated receptor (TNFR1), and cytochrome-c oxidase (COX) were suggested as playing an important role in porcine atresia. Present study also enlists key upstream regulators in follicle atresia based on our results and on a literature review. The novel gene candidates and gene networks identified in the current study lead to a better understanding of the molecular regulation of ovarian follicular atresia.