During the first meiotic prophase of mammalian spermatogenesis, the sex chromosomes generally undergo a transient process of transcriptional inactivation called meiotic sex chromosome inactivation (MSCI). This process is initiated shortly after the formation of meiotic double-strand breaks (DSBs), when DNA damage response proteins accumulate on these unsynapsed chromosomes, triggering local chromatin changes. However, recent studies have shown that MSCI is not a complete process, as 80% of X-linked miRNA genes manage to escape it. While the observation that these miRNAs are mostly found in multiple copies suggests a possible role for homologous recombination based repair in allowing evasion from the silencing machinery, so far what allows genes to escape MSCI remains unkown. Using RNA-sequencing data for three mouse spermatogenic cell types, we observe that the response of X-linked protein-coding genes to MSCI is highly variable. To explain this variability, we analysed the contribution of several gene characteristics, including their ability to avoid and repair DSBs, their evolutionary age, and the level of post-transcriptional regulation their transcripts are submitted to. Finally, we generated a linear model capable of explaining 35% of the observed gene expression variability during MSCI.