Splicing and alternative splicing are involved in the expression of most human 
genes, playing key roles in differentiation, cell cycle progression, and 
development. Misregulation of splicing is frequently associated to disease, 
which imposes a better understanding of the mechanisms underlying splicing 
regulation. Accumulated evidence suggests that multiple trans-acting factors and 
cis-regulatory elements act together to determine tissue-specific splicing 
patterns. Besides, as splicing is often cotranscriptional, a complex picture 
emerges in which splicing regulation not only depends on the balance of splicing 
factor binding to their pre-mRNA target sites but also on 
transcription-associated features such as protein recruitment to the 
transcribing machinery and elongation kinetics. Adding more complexity to the 
splicing regulation network, recent evidence shows that chromatin structure is 
another layer of regulation that may act through various mechanisms. These span 
from regulation of RNA polymerase II elongation, which ultimately determines 
splicing decisions, to splicing factor recruitment by specific histone marks. 
Chromatin may not only be involved in alternative splicing regulation but in 
constitutive exon recognition as well. Moreover, splicing was found to be 
necessary for the proper 'writing' of particular chromatin signatures, giving 
further mechanistic support to functional interconnections between splicing, 
transcription and chromatin structure. These links between chromatin 
configuration and splicing raise the intriguing possibility of the existence of 
a memory for splicing patterns to be inherited through epigenetic modifications.