LH induces ovulation, COC expansion, oocyte maturation, and luteinization in preovulatory follicles. These events are mediated by LH activation of the PKA pathway and NRIP1, which induce the expression of the EGF-like factors (AREG, EREG). AREG and/or EREG in turn activate the EGFR signaling cascade, including RAS and ERK1/2. This hypothesis is based on the observations that when Erk1 and Erk2 are disrupted in granulosa cells, global changes occur in gene expression patterns that control ovulation, COC expansion, resumption of meiosis, and luteinization. Moreover, activation of ERK1/2 is essential to turn off the FSH-regulated gene expression program that controls genes essential for preovulatory follicle growth and differentiation. C/EBPα and C/EBPβ, NR5A2 (also known as LRH1), and possibly PGR appear to be among the key transcription factors that are activated by ERK1/2 phosphorylation and affect ovulation and luteinization. Other transcription factors that are targets of ERK1/2 include members of the AP1 family and EGR1/3, whose specific functions in ovulation and luteinization remain to be defined. Additionally, oocyte-derived factors such as GDF9 and BMP15 affect cumulus cell and granulosa cell functions in a gradient-dependent manner. The functions of specific genes are discussed in the text. TK, tyrosine kinase.